Preparations for stimulating visual functions in various degenerative diseases of the retina and neuropathies. Neuroprotectors in the treatment of glaucoma - review of drugs

Ophthalmologists are well aware of the fact of a decrease in visual function due to the progression of glaucoma against the background of normalized (medically, surgically or laser ophthalmotonus), which is diagnosed in 18-60% of cases, more often in patients with somatic pathology, especially when there is a triad or tetrad concomitant diseases.

The deterioration of visual functions is associated with a cascade of secondary events caused by progressive damage to retinal ganglion cells (RGCs) due to disturbances in regional and general hemodynamics, changes in the hemomicrocirculation system in the posterior segment of the eye, the aggregation state of the blood, affecting the level of blood supply to the optic nerve (ON) and accumulation of toxic substances in neurons - glutamate, free radicals, nitrooxides, etc. There are also indications of the important role of intraocular fluid as a factor in the trophism and metabolism of the retina and optic nerve.

Since involutional and metabolic disorders, general vascular diseases, changes in cerebral circulation, and a decrease in the activity of the antioxidant system are of great importance in the pathogenesis of glaucoma, then to prevent or at least slow down the processes of apoptosis of GCS in patients with glaucoma, in addition to local hypotensive treatment, regular general treatment is necessary, which should be complex with an effect on improving the trophism of the tumor, the conductivity of nerve fibers, reducing the negative effects of peroxides, or various methods of influence, taking into account the stage and course of the disease.

In addition to medication, physiotherapeutic and surgical methods are used using vasoreconstructive, decompression, extrascleral and revascularization interventions. To improve the bioavailability and effectiveness of a number of drugs, methods of “targeted” delivery of drugs to the choroid and optic nerve are also used - catheterization of the retrobulbar space, sub-Tenon infusion system, trophic sclerectomy, etc.

An important and integral part of the complex treatment of unstabilized primary open-angle glaucoma (POAG) stages I-III with normalized intraocular pressure (IOP) is currently considered mandatory neuroprotective therapy aimed at preserving visual functions (VF) by preventing further loss of RGCs and increasing the tolerance of ON to increased load. Of the drugs that have a neuroprotective effect, the most widely used are antioxidant, vasodilator, nootropic drugs, NMDA receptor blockers, neuropeptides, etc.

Primary neuroprotectors, whose action is aimed at interrupting the earliest processes of the glutomat-calcium or ischemic cascade, include NMDA receptor antagonists, such as, for example, memantine, magnesium and glycine. The most promising of them seems to be memantine, clinical observations of the use of which indicate an improvement in functional indicators in patients with POAG after 3 weeks of use of the drug.

Calcium channel blocker drugs, which are also primary neuroprotectors, include cinnarizine, stugeron, nifedipine, nimodipine, verapamil, norvasc, amlodipine, etc., which also have vasoactive and local hypotensive effects. According to N.I. Kurysheva, the mechanism of action of antagonists of voltage-dependent calcium channels may involve calcium blockade - induced toxicity, leading to the death of retinal neurons in the process of the glutamate-calcium cascade.

Secondary direct neuroprotectors that act preventively and the use of which is more preferable, given the course and long-term nature of the treatment of glaucomatous optic neuropathy (GON), include antioxidants, neuropeptides, agents that improve ocular hemodynamics in glaucoma, peptide bioregulators, etc. To correct metabolism, such antioxidants and antihypoxants such as emoxipin, mexidol, vitamin E, aevit, histochrome, riboxin, cytoflavin, Lutein complex (flavonoids, vitamin A, beta-carotene, zinc, copper - components of superoxide dismutase), etc., which also have antiaggregation and antiprotective properties.

Neuropeptides play an important role in the functioning of nervous tissue, the most typical example of which is Cerebrolysin, clinical studies of which have confirmed its high effectiveness in the treatment of central chorioretinal dystrophies. Particular attention is paid to the domestic neuropeptide - Semax, the use of which in the form of endonasal electrophoresis (10 sessions) and subsequent intranasal instillation for 3 weeks ensured stabilization and even improvement of clinical and functional parameters, rheological properties of blood and ocular hemodynamics in patients with unstabilized glaucoma and normalized IOP .

As is known, in the pathogenesis of GON, much attention is paid to the vascular factor, and in this context, drugs that improve ophthalmohemodynamics should be noted. Typical representatives of such drugs are no-spa and papaverine. To improve collateral blood circulation, agents are used that improve microcirculation and have an antiaggregation effect (aspirin, trental, gingko biloba - tanakan).

To stabilize the glaucomatous process in complex therapy, beta-blockers are also used - obzidan, statins that lower blood lipids and have an anti-sclerotic effect - atorvastatin, mevacor, clofibrate, miscleron, etc., cardio- and angioprotector, antihypoxant - mildronate, incl. based on sub-Tenon implantation of bioalloplant. To correct metabolic disorders and stop the progression of the glaucomatous process, I. N. Beskorovainaya et al. successfully used a solution of corvitin, a bioflavonoid and capillary stabilizer that also has antioxidant and immunomodulatory properties. Piracetam also has the ability to improve metabolic processes in nervous tissue, improving the rheological properties of blood.

Some researchers have noted a clear positive effect from the use of nootropic drugs in complex therapy: noben, gliatiline-choline alfoscerate, citicoline in the form of daily IV infusions for 10 days, followed by oral use for 20 days. When taking the nootropic drug phenotropil for a month at 100 mg 1 time per day and target IOP, stabilization of the process was noted within 6 months in 80% of patients.

According to V.V. Egorov, the basis of the treatment complex for unstabilized POAG with compensated IOP should be: calcium channel antagonists (cinnarizine), drugs that improve the energy parameters of the heart and increase resistance to the damaging effects of toxic metabolites of lipid peroxidation (riboxin), a corrector of sympatho- adrenal system, peptide bioregulator - epithalamin, magnetic laser stimulation of the cervical and carotid sympathetic ganglia. The identified features make it possible to predict the course of POAG and adjust the treatment regimen.

In recent years, peptide bioregulators or cytomedins have become widespread, which in some cases are used in isolation, in others - in complex traditional treatment. The best effect was recorded with the combined use of cortexin (IM) and retinalamin (p/b), as well as with monotherapy with retinalamine when administered into the sub-Tenon's space or through a catheter installed in the retrobulbar space. More economical, but no less effective, is the administration of retinalamin or cortexin by endonasal electrophoresis.

Kh. S. Ashirmatova et al. S/W administration of retinalamin is combined with lymphotropic (injections of anesthetic, antioxidant and metabolic) and traditional therapy. After six months, stabilization of visual functions was noted in 88% of POAG II and in 60% of stage III. The use of retinalamin is also advisable in combination with fistulizing operations for POAG or drainage surgery for refractory glaucoma. Some authors note a pronounced and prolonged neuroprotective effect from collagenoplasty of the sclera with xenoplast material impregnated with retinalamine (expansion of the visual field by 78.4%). Another effective combination is the use of intramuscular injections of cortexin and transcorneal magnetic therapy. At the same time, stabilization of MN parameters was noted in 73%.

L. G. Aligadzhieva et al. We used retroscleroplasty with the introduction of Alloplant biomaterial into the sub-Tenon space in combination with a course of vascular-metabolic therapy (sub injections of retinalamine, intravenous injections of Mexidol, Actovegin, intramuscular injections of emoxypine and administration of Aevit, Gincobeloba).

The best treatment results were obtained from the combined use of epithalamin biopeptide and intravascular laser irradiation of blood, included in a course of therapy (10 days) for unstabilized POAG with normalized IOP. The effect lasted up to 6-8 months, whereas after traditional treatment it lasted no more than 3 months. V. A. Nepomnyashchikh, M. A. Kadyshev report on the advisability of the combined use of the peptide regulator “Connectisan A” (with sub-Tenon administration or magnetophoresis) and vasoactive antihomotoxic drugs in the complex therapy of unstabilized POAG with normal IOP.

Courses of neuroprotective therapy should not be carried out less than 1-2 times a year. According to L.A. Sukhina et al. (2010), however, even regular such courses in patients with advanced glaucoma did not prevent a narrowing of the total visual field (OV) in 91% of patients when they were observed for 6 years. The combination of neuroprotective therapy with revascularization surgery turned out to be more effective (narrowing of the visual field in only 39%).

Shmyreva V.F. and Mostovoy E.N. (2001) studied the neuroprotective effectiveness of operations on the scleral canal of the optic nerve in combination with cell therapy. Autologous activated leukocytes in the form of a suspension of cells in blood serum were injected into the area of ​​discision (0.1-0.2 ml). Up to 2 years after this treatment, the authors observed an expansion or stabilization of the boundaries of the PV, an increase in perfusion pressure, and a decrease in the depth and area of ​​MN excavation.

A number of authors consider one of the most promising areas of neuroprotection to be the simultaneous combined effect of physical factors with mutual potentiation of their therapeutic effect. In particular, L.F. Linnik et al. assessed the effectiveness of using simultaneous magnetic and transcutaneous electrical stimulation against the background of drug therapy in the treatment of patients with unstabilized POAG and normalized IOP. Expansion of the PV was noted in 86%, an improvement in electrophysiological parameters - in 88-93%, an increase in the linear velocity of blood flow in the orbital artery - in 78%, and the initial effect remained stable in 67% for 6 months. T. G. Kamenskikh et al. transcranial magnetic therapy and electrical stimulation were performed on the Amo-Atos-E apparatus for 20 minutes for 10 days. The method made it possible to improve the DF and activate hemodynamics in the vascular system of the eye.

N. A. Shigina et al. (2008) believe that stabilization of the glaucomatous process in patients with normalized IOP can be achieved using a set of measures consisting of homotoxicological and cellular methods in combination with physiotherapeutic methods. A. I. Bereznikov and V. M. Sheludchenko proposed a method of electropharmacostimulation of the optic nerve for the treatment of unstabilized POAG with normalized IOP, which consists of repeated (4-6 times a day) administration of drugs (vasodilators, antioxidants, etc.) and Once a day - 10% piracetam solution through a catheter installed in the retrobulbar space, and after 40 minutes - electrical stimulation. Improvement in visual acuity was achieved in 62%, and expansion of visual acuity in 80% of patients. Electropharmacostimulation using a solution of solcoseryl was reported by A. I. Bereznyakov et al. . According to the authors, the effectiveness of such treatment is more effective than using piracetam.

M. I. Aleshaev, N. B. Shurupova use lymphotropic therapy in the mastoid area with heparin and emoxipine (10 injections, once every six months), which ensured stabilization of the process in 84% of cases, which is significantly higher compared to the control group (emoxipine p/b and nicotinic acid w/o) - 40%.

It is known to use color pulse therapy in the postoperative period of patients with POAG, which increases the effect of standard conservative treatment. Having applied this method (stimulation was carried out on the ADFT-4 apparatus in blue in the range of 15 Hz, course - 14 days), G. Sh. Abizgildina noted its positive effect on the hemo- and hydrodynamics of the eyes, which persisted for 3 months. The results of combined optical reflex and color pulse therapy on the Visotronic M3 simulator turned out to be even more effective, which made it possible to improve visual functions and significantly reduce IOP. Acupuncture also turned out to be useful, the long-term results of which revealed the persistence of the effect for 3-6 months.

conclusions. The path to effective treatment of unstabilized glaucoma with normalized IOP lies in the selection of several drugs or methods of influencing various parts of the pathogenesis of GON, which will enhance the neuroprotective effect and reduce the risk of undesirable side effects. As for surgical methods for correcting ocular hemodynamics (decompression of the optic nerve, choroidal revascularization in various modifications, ligation of the facial branches of the external carotid artery, etc.), clear indications for their use have not yet been developed, and effectiveness is not always indicative.

25-06-2012, 21:09

Description

Tanakan (Tanakari)

The drug belongs to angioprotectors and is a microcirculation and cerebral circulation corrector. Improves the rheological properties of blood. Improves peripheral, including cerebral, circulation, oxygen supply to the brain, inhibits platelet activating factor, and inhibits the aggregation of blood platelets. Has antihypoxic and anti-edematous effects, prevents the formation of free radicals and lipid peroxidation of cell membranes. Affects the release, reuptake, catabolism of neurotransmitters and their interaction with receptors. The first signs of improvement appear 1 month after the start of treatment.

Indications:

• encephalopathy (after a stroke, traumatic brain injury, in old age, alcoholic origin), manifested by attention and/or memory disorders, decreased intellectual abilities, sleep disorders;
• disorders of peripheral circulation and microcirculation, including arteriopathy of the lower extremities, Raynaud's syndrome;
• neurosensory disorders (dizziness, tinnitus, hypoacusia, sclerotic macular degeneration, diabetic retino- and polyneuropathy);
• asthenic conditions (psychogenic, caused by brain injuries, neurotic depression).

Dosages: 40 mg orally during meals (for asthenic disorders - 80 mg) 3 times a day. The course of treatment is 1-3 months. When the course of treatment is extended to 6 months, a stable therapeutic effect is achieved for up to 1 year.

Side effects: rarely - dyspeptic symptoms, headache, allergic skin reactions.

Contraindications: not identified.

Compound: 1 film-coated tablet contains standardized ginkgo biloba extract 40 mg; 1 ml of oral solution - 40 mg; in 30 ml bottles complete with a dosing pipette. Manufactured by Beaufour Ipsen International, France.

Theophylline ethylenediamine (Theophylline nicotinas)

Is antispasmodic. Reduces platelet aggregation, improves eye microcirculation, increases the activity of antioxidant systems when used in combination with nicotinic acid.

Dosages: orally after meals, 1 tablet 3 times a day. The duration of therapy is several months. Theophylline 250 mg 3 times a day for 2 weeks. Intravenously 1 time per day, 600-800 mg, course of treatment is 2 weeks.

Side effects: hypotension, palpitations, gastrointestinal disorders, dizziness.

Contraindications: acute myocardial infarction, tachyarrhythmias, arterial hypertension, peptic ulcer of the stomach and duodenum, hypersensitivity.

Drugs

• Eufillin (aminophylline) tablets of 150 mg, 30 pieces in a package. Manufactured by Olainfarm, Latvia; Akrikhin, Russia.
• Euphylong (theophylline)) retard capsules of 250 mg, in packages of 50 and 100 mg. Manufactured by Byk Gulden, Germany.
• Theophylline nicotinate(xanthinol nicotinate) tablets 150 mg, 10 pieces in a package. Manufactured by Akrikhin, Russia. Ampoules of 2 ml of 15% solution, in a package of 10 pieces. Produced by Akrikhin, Russia; ICN, USA.

Cavinton

Refers to antispasmodics. It has antihypoxic effectiveness, restores energy balance due to the accumulation of ATP, and reduces platelet aggregation.

Dosages: 1-2 tablets 3 times a day for a month. Intravenous drip (2 ampoules are diluted in 500 ml of physiological solution).

Side effects: hypotension, palpitations.

Contraindications: IHD, severe forms of arrhythmia, hypersensitivity.

A drug

• Cavinton (vinpocetine) 5 mg tablets, 50 pieces in a package; ampoules of 2 ml, 1 ml contains 5 mg of Cavinton. Manufactured by Gedeon Richter, Hungary.

Pentoxifylline (Pentoxyphillinum)

Improves microcirculation and rheological properties of blood. Has a vasodilating effect.

Dosages: tablets 400 mg 3 times a day, course 1 month. Intravenously, 5 ml in 500 ml of saline.

Side effects: gastrointestinal disorders, dizziness.

Contraindications: acute myocardial infarction, massive bleeding, retinal hemorrhage. Diabetic retinopathy.

Drugs

• Trental 5 ml each, 5 ampoules per pack. Manufactured by Hoechst Marion Roussel, India; Hoechst, Germany.
• Pentilin tablets 400 mg, 20 pieces in a package. Manufactured by KRKA, Slovenia.

Dipyridamole (Dipyridamolum)

The drug improves microcirculation, is an antiplatelet agent, and an angioprotector.

Dosages: orally before meals, drink with plenty of water. The duration of therapy and dosage depend on the severity of the disease and the patient's response to the drug.

Side effects: hypotension, dizziness, facial flushing, nausea, rash.

Contraindications: acute myocardial infarction, unstable angina, collapse, severe renal dysfunction.

A drug

• Chimes 25 mg and 75 mg, in packs of 100 and 40 pieces. Manufactured by Berlin-Chemie, Germany.

Cinnarizin (Cinnarisinum)

Calcium channel blocker, improves cerebral and peripheral circulation, reduces the tone of smooth muscles of arterioles. Increases tissue resistance to hypoxia.

Dosages: orally before meals, 1-2 tablets three times a day.

Side effects: drowsiness, dry mouth, dyspepsia.

Contraindications

Drugs

• Cinnarizine 25 mg tablets, 50 pieces in a package. Manufactured by Akrikhin, Russia.
• Cinnasan 75 mg capsules, 50 pieces per pack. Manufactured by Sanofi, France.
• Stugeron 25 mg capsules, 50 pieces per pack. Manufactured by Gedeon Richter, Hungary.

Adrusen Zinko

Restores the functions of the body's enzymatic systems, which prevent the processes of premature aging of tissues by suppressing the phenomena of pathological lipid peroxidation in tissues (in the retina, lens, cornea, gonads, cells of the nervous system), slows down the increase in the phenomena of vascular atherosclerosis and degenerative manifestations of joint damage.

Indications: Adruzen Zinco is indicated for retinal dystrophy, incipient cataracts, retinopathy of various origins, visual fatigue, diabetes mellitus and its complications. The drug is used as an adjunct in the treatment of diseases in the pathogenesis of which processes of decompensated free radical oxidation of tissue lipids are noted:

• with increased physical and physiological stress (pregnancy);
• asthenic condition (especially in old age);
• with sensorineural hearing loss;
• lipid metabolism disorders and progression of coronary heart disease;
• for hormonal dysfunction, psoriasis and neurodermatitis;
• in cosmetology; for autoimmune and metabolic diseases of the joints (improving the elasticity of connective tissue);
• in the recovery period after chemotherapy and radiation therapy.

Dosages: Take 1 capsule 2 times a day between meals and wash down with 1/2 glass of water. Maintenance dose- 1 capsule per day. For dyspeptic symptoms of a functional nature, administration is possible 15-20 minutes after eating. The course of taking Adruzen Zinco is from 4 weeks to 3-6 months.

Contraindications: not identified.

Undesirable effects: sometimes transient dyspeptic disorders in the form of belching and drooling are detected.

Compound: “special form” of zinc 27 mg (equivalent to 66.7 mg zinc sulfate or 75 mg zinc acetate); selenium - 0.75 mg; copper - 1 mg; vitamin E (alpha tocopherol) - 10 mg; omega-3 acids - 125 mg (polyunsaturated essential fats in the optimal biologically active ratio), obtained by sublimation. Manufactured by S.I.F.I., Italy.

Mirtilene Forte

Dry extract from blueberries contains antho-cyanoside 177 mg.

Anthocyanosides extracted from blueberries enhance the regeneration of the light-sensitive pigment rhodopsin and thus improve the sensitivity of the retina to various levels of light radiation, enhancing visual acuity in low light. The angioprotective effect of anthocyanosides on capillaries is used in cases of changes in the retina in diabetes mellitus. Mirtilene Forte reduces capillary fragility, restoring their patency, improves microcirculation of the retina and, accordingly, reduces the adverse manifestations of diabetic microangiopathy. Inhibits the activity of the enzyme aldose reductase, which causes the formation of sorbitol in tissues, which is responsible for the development of cataracts and retinopathy in diabetics.

Indications:

• myopia (moderate and high myopia), acquired hemeralopia.
• Diabetic retinopathy.
• Diabetic cataract.
• Violation of the mechanisms of vision adaptation to darkness during night (scotopic) and twilight (mesopic) vision.
• Visual fatigue.
• Retinal dystrophy.
• Muscular asthenopia.

Dosages: 3 capsules per day or as directed by a physician.

Contraindications: hypersensitivity to any component of the drug.

Undesirable effects: The drug is well tolerated in recommended doses.

Compound: the drug, in addition to blueberry extract, contains other ingredients: soybean vegetable oil; vegetable hydrogenated fats; gelatin; glycerol; iron oxide red; iron oxide black; sodium ethyl oxybenzoate; sodium propyl oxybenzoate. The blister contains 20 capsules of 177 mg each. Manufactured by S.I.F.I., Italy.

Strix

Has a retinoprotective effect. Restores visual purple, strengthens eye capillaries, enhances visual acuity (including in patients with complicated myopia), reduces asthenopic syndrome, improves twilight vision.

Indications:

• fatigue and pain in the eyes, eye fatigue from working with a computer, reading, wearing contact lenses, bright lighting, long driving at night;
• complex treatment of eye diseases (as recommended by a doctor): primary glaucoma, the period after antiglaucomatous operations, diabetic retinopathy, central and peripheral chorioretinal dystrophies, complicated myopia, asthenopia, visual fatigue syndrome, impaired vision adaptation to darkness.

Dosages: orally with 1 glass of water, usually 1 tablet. 2 times a day for 2-3 weeks or as needed immediately before visual stress. Primary glaucoma (as part of complex treatment): 2 tables. 1 time per day for 1 - 1.5 months.

Compound: 1 tablet contains bilberry extract 260 mg (corresponding to the content of 12 mg of anthocyanosides) and beta-carotene 1.2 mg. Blister contains 30 pcs. Made by Ferrosan, Denmark.

Piracetam

Has antihypoxic and antioxidant effects. Strengthens the energy activity of the brain. Stimulates mental performance. Improves neurometabolism.

Dosages: 1 tablet orally 3 times a day. The course of treatment is up to 2 months. Intramuscularly or intravenously up to 6-8 g per day, course 10-14 days. Capsules 0.4 g 3 times a day, up to 6 months.

Side effects: nervousness, excitement, irritability.

Contraindications: hypersensitivity to the drug, severe renal dysfunction.

Drugs

• Piracetam (nootropil) tablets 400 mg, 60 pieces in a package. Manufactured by Polpharma, Poland; Akrikhin, Russia.
• Nootropil capsules 400 mg each, in a package of 60, 30 or 20 pieces. Solution for injection, 60 ml in a dropper bottle; injection solution 20%, 5 ml in ampoule, 4 pieces per package. Manufactured by UCB, the Netherlands.

Adenosine triphosphoric acid (Acidum adenosintriphosphoricum)

Antihypoxant. Strengthens cerebral and coronary circulation, reduces tissue hypoxia by increasing the activity of Krebs cycle enzymes.

Dosages: intramuscularly 1 ml once a day, course of treatment up to 1-2 months.

Side effects

Contraindications: IHD, liver diseases.

A drug

• Sodium adenosine triphosphate solution(ATP) ampoule of 1 ml of 1% solution, 10 pieces in a package. Manufactured by Akrikhin, Russia.

Riboxin (Riboxinum)

Antihypoxant. Strengthens cerebral and coronary circulation, reduces tissue hypoxia by increasing the activity of Krebs cycle enzymes. Plays an important role in exchange processes.

Dosages: Tablets 0.2 g 3 times a day, course of treatment up to 1 year. Intravenous 2% solution, 5 ml, 5-10 injections.

Side effects: allergic reactions, exacerbation of gout.

Contraindications: IHD, liver diseases.

Drugs

• Riboxin in ampoules 2% solution of 5 ml. Made in Akhrikhin, Russia.
• Riboxin (inosine) tablets of 200 mg, packages of 30 and 50 pieces. Manufactured by Veropharm, Russia.

Cytochrome C

Refers to cytoprotectors. It is an enzyme preparation that affects tissue metabolism.

Dosages: 2 tablets 4 times a day. Intravenously, 15 ml 1-2 times a day.

Side effect: allergic reactions.

Contraindications: hypersensitivity.

A drug

• Cytochrome C ampoules of 1 ml of solution contain 2.5 mg in a 4 ml bottle, 10 bottles in a package; tablets of 0.01 g, in a package of 50 pieces. Manufactured by Heinrich Mack, Germany.

Wobenzym

• It has immunomodulatory, anti-inflammatory, anti-edematous, fibrinolytic, antiplatelet effects.
• Has a positive effect on the course of the inflammatory process.
• Limits the pathological manifestations of autoimmune and immune complex processes.
• Accelerates the lysis of toxic metabolic products and dying tissues.
• Improves the resorption of hematomas and edema.
• Reduces the permeability of vascular walls.
• Improves the rheological properties of blood and microcirculation, increases the supply of tissues with oxygen and nutrients.
• Increases its own fibrinolytic potential.
• Has a secondary analgesic effect.

Indications: atopic dermatitis, multiple sclerosis, post-thrombotic syndrome, vasculitis, thromboangiitis obliterans, post-traumatic edema, oncological diseases, plastic and reconstructive surgery, etc.

Dosages: orally 30 minutes before meals, without biting, with a glass of water (150 ml) - 3-10 tablets. 3 times a day.

• With high disease activity - 7-10 tablets. 3 times a day for 2-3 weeks, then the dose is reduced to 5 tablets. 3 times a day for 2-3 months.
• With average disease activity - 5-7 tablets. 3 times a day for 2 weeks, then 3-5 tablets. 3 times a day for 2 weeks.
• To increase the effectiveness of antibiotic therapy and prevent dysbiosis, 5 tablets are used throughout the entire course of antibiotic therapy. 3 times a day.
• After stopping the course of antibiotics to restore the intestinal microflora (biocenosis) - 2-3 tablets. 3 times a day for 2 weeks.

• As cover therapy during chemotherapy and radiation therapy - 5 tablets each. 3 times a day until the end of the course.
• In order to prevent diseases and improve the quality of life - 2-3 tables. 3 times a day, course - 1.5 months, repeated 2-3 times a year.
• For chronic diseases, Wobenzym can be used in long courses from 3 to 6 months or more.

Side effects: skin rashes (urticaria).

Contraindications: hemophilia, thrombocytopenic purpura. Individual intolerance to the drug.

Use during pregnancy and breastfeeding: Pregnant women and nursing mothers should take Wobenzym only under the supervision of a physician.

Interaction: increases the concentration of antibiotics in the blood plasma and the site of inflammation.

Precautionary measures: If side effects or allergic reactions occur, stop taking the drug and consult a doctor.

special instructions: resistant to gastric juice. For infectious and inflammatory diseases, it does not replace antibiotics, but increases their effectiveness and reduces side effects.

Compound: 1 tablet, coated with a coating resistant to gastric juice, contains bromelain 45 mg, papain 60 mg, pancreatin 100 mg, chymotrypsin 1 mg, trypsin 24 mg, amylase 10 mg, lipase 10 mg and rutoside 50 mg; in a blister of 20 pcs., in a box of 2 or 10 blisters, or in bottles of 800 pcs. Manufactured by Mucos Pharma (Germany).

Emoxipinum (Emoxipinum)

• It has antiplatelet, antihypoxic, angioprotective effects.
• Reduces the permeability of the vascular wall, blood viscosity and coagulability, and the ability of platelets to stick together.
• Strengthens the process of fibrinolysis.
• Improves microcirculation.
• Protects the retina from the damaging effects of high-intensity light, promotes the resorption of intraocular hemorrhages.
• Increases the brain's resistance to hypoxia and ischemia, normalizes tissue metabolism (including during stroke and myocardial infarction).
• Has a pronounced cardioprotective effect.
• Effective for conditions accompanied by increased lipid peroxidation (including skin diseases, glaucoma, etc.).

Indications:

• intraocular hemorrhages,
• diabetic retinopathy,
• central chorioretinal dystrophy,
• thrombosis of the central retinal vein and its branches,
• post-traumatic hemorrhages,
• complicated myopia,
• protection of the retina of the eye when exposed to high intensity light (laser and sunburn, laser coagulation),
• glaucoma (in the postoperative period).

Dosages:

• in ophthalmology, a 1% solution of emoxypine is used, 1-2 drops are installed into the conjunctival sac 2-3 times a day for 2-30 or more days, retrobulbar - 0.5 ml of a 1% solution 1 time a day for 10- 15 days;
• parabulbar and subconjunctival - 0.2-0.5 ml 1 time per day for 10-30 days;
• to protect the retina during laser coagulation - retrobulbar 0.5 ml per day and 1 hour before the procedure, then retrobulbar 0.5 ml for 2-10 days, once a day.

Side effects: excitement (short-term) drowsiness, increased blood pressure, rash, local reactions: pain, burning sensation, itching, redness, hardening of paraorbital tissues.

Contraindications: hypersensitivity, pregnancy.

Precautionary measures: It is necessary to constantly monitor blood pressure and blood clotting.

The drug is available in the form of a 1% solution in 5 ml bottles and 1 ml ampoules.

Production: Moscow Endocrine Plant, Russia.

Erisod

Refers to antihypoxants. A drug improves the body's utilization of oxygen and reduces the need for it in organs and tissues, the drug is an enzyme superoxide dismutase (SOD), isolated from human erythrocytes. SOD prevents damage to cell membrane lipids.

Indications: various dystrophic diseases of the anterior segment of the eyeball and retina; neuropathy.

Dosages: 1 drop 4-6 times a day into the affected eye.

Side effects: allergic reactions.

Contraindications: hypersensitivity to the drug.

A drug

• Erisod eye drops of 1,600,000 units and 400,000 units, 10 ampoules per package. Manufactured by RESBIO, Russia.

Article from the book: .

Neuroprotection involves protecting the retina and optic nerve fibers from the damaging effects of various factors, primarily from ischemia. Neuroprotective therapy is aimed at correcting metabolic disorders that occur with glaucoma in the head of the optic nerve, improving local microcirculation and tissue trophism, and normalizing the rheological properties of blood.

Currently, it is customary to distinguish two groups of neuroprotective drugs - direct and indirect action.

Direct-acting neuroprotectors directly protect retinal neurons and optic nerve fibers by blocking direct factors of cell damage that cause an increase in the concentration of lipid peroxidation products (LPO) and free radicals, Ca++ ions, and acidosis.

Neuroprotectors of indirect action, influencing various pathophysiological disorders (decrease in perfusion pressure, atherosclerosis, changes in the rheological properties of blood, vasospasm) and increasing the resistance of various functional systems to a decrease in oxygen perfusion pressure in tissues, indirectly have a protective effect. Drugs that improve microcirculation, rheological properties of blood, reduce cholesterol levels in the blood, and nootropic drugs have a similar effect.

Neuroprotective therapy should always be carried out with active antihypertensive treatment (medical, laser or surgical) to achieve target pressure.

It should be noted that the classification of drugs according to the nature of their neuroprotective effect in glaucoma is very conditional, because Not all mechanisms of action are well studied, and the mechanism of apoptosis of retinal ganglion cells in glaucoma is largely based on theoretical assumptions.

4.7.1. Calcium channel blockers

Today, there is information about the existence of several types of ion channels, as well as various drugs that block the entry of Ca++ ions into the cell through these channels. Calcium channel blockers not only increase cell resistance to ischemia, but also have a vasodilatory effect. Among the drugs in this group, the selective b-blocker - betaxolol (Betoptik, Betoptik S) - attracts the greatest attention of ophthalmologists (see subsection 4.3.1.1.2).

4.7.2. Enzyme antioxidants

SUPEROXIDE DISMUTASE (SOD) (ERISOD)

pharmachologic effect

It is a natural component of the body's antioxidant defense. By causing the destruction of reactive oxygen species, SOD has antioxidant and anti-inflammatory effects. SOD, due to its pronounced antioxidant effect, inhibits the development of degradation processes in trabecular tissue and optic nerve fibers.

SOD penetrates well into various eye tissues using various methods of administration. The maximum concentration of the drug is determined after 60-120 minutes. The drug accumulates best in the choroid and retina. The highest concentrations of the drug in the retina are observed with instillation and subconjunctival administration. The rate of removal of SOD from the eyeball depends on the method of administration and the structure of the eyeball under study. On average, the half-life is about 2 hours.

Dosage regimen

The most appropriate instillation of the drug is administered 5-6 times a day. It is also possible to use the forced instillation method - within an hour, 1 drop of the drug is instilled 6 times with an interval of 10 minutes. The course of treatment is 2-4 weeks, the interval between courses is 2 months.

Contraindications

Individual hypersensitivity to the components of the drug.

Local side effect

Rarely burning, irritation.

Systemic side effect

Allergic reactions may develop.

I. Basic principles of local antihypertensive therapy

1. Reducing the level of IOP to prevent further irreversible progression of visual impairment.

2. Achieving the “goal pressure” (on average, reducing the IOP level by 20-30% from the initial level). Moreover, the more damage is caused to the optic nerve, the lower the level of “target pressure” should be. Regular monitoring of the correspondence of tonometric pressure to the “target pressure” is necessary.

The upper limit of the desired ophthalmotonus corresponds to:

at the initial stage, true IOP (P0) is 18-20 mm Hg. Art. (tonometric IOP (P t) 22-24 mm Hg);

at an advanced stage, the true IOP (P0) is 15-17 mm Hg. (tonometric IOP (P t) 19-21 mm Hg);

at an advanced stage, the true IOP (P0) is 10-14 mm Hg. (tonometric IOP (P t) 16-18 mm Hg).

3. Drug treatment must be effective and sufficient to reliably control IOP levels. In this case, one should remember about the so-called effect of tachyphylaxis (i.e., addiction to drugs) and the need for timely correction of the therapy when the slightest signs of IOP subcompensation are detected.

4. The Russian pharmaceutical market contains almost all pharmacological groups of antiglaucomatous drugs that have become widespread in the world. In this regard, the doctor has the opportunity to make a pathogenetically substantiated choice of drug, based, first of all, on data on its clinical effectiveness.

5. Constantly keeping in mind the need to achieve effective treatment and having the opportunity to choose a drug, you should pay attention to the so-called “cost-effectiveness” criterion. This criterion allows you to take into account and compare the costs and effectiveness of the prescribed therapy. Often, initially more expensive drugs are ultimately more beneficial for patients, including due to a more effective and controlled decrease in IOP levels.

II. General principles for choosing antihypertensive drug therapy

1. Before treatment, the expected “target pressure” is determined taking into account all the risk factors present in this particular patient.

2. Treatment begins with monotherapy with the drug of first choice. If it is insufficiently effective, this drug is replaced with another drug from another pharmacological group; if in this case it is not possible to achieve an adequate reduction in IOP, then they move on to combination therapy.

3. If there is intolerance or there are contraindications to the use of the selected drug, treatment begins with the use of another drug.

4. When carrying out combination therapy, you should not use more than two drugs at the same time; It is preferable to use combined drugs.

5. When carrying out combination therapy, you should not use drugs belonging to the same pharmacological group (for example, you cannot combine two different b-blockers or two different prostaglandins).

6. The adequacy of the achieved hypotensive effect is regularly checked by the dynamics of visual functions and the condition of the optic nerve head.

7. When assessing drug exposure, the following must be taken into account:

· type of influence on the hydrodynamics of the eye;

· degree of possible reduction in IOP;

· contraindications for use;

· portability;

· required frequency of use.

The last two factors can significantly worsen the quality of life of patients and, ultimately, lead to non-compliance with the recommended treatment regimen, which reduces the effectiveness of the therapy.

8. When choosing a drug, a systematic comparison of the obtained tonometric pressure with the “target pressure” is necessary. The IOP should not be higher than the “target pressure”.

9. Treatment is carried out throughout the patient’s life. When carrying out drug therapy, it is advisable to change medications. For this purpose, therapy is changed 2-3 times a year for 1 month, with the exception of therapy with prostaglandins and carbonic anhydrase inhibitors. Replacement should be carried out with a drug belonging to another pharmacological group.

III. Requirements for an ideal drug for the treatment of glaucoma

The drug should:

1) effectively reduce intraocular pressure;

2) maintain a low level of IOP with slight fluctuations in its values ​​throughout the day;

3) maintain its hypotensive effect for a long time;

4) have a minimum of adverse reactions;

Neuroprotective therapy in the treatment of primary open-angle glaucoma with compensated intraocular pressure

Primary open-angle glaucoma (POAG) remains a serious health problem in all countries of the world, requiring large financial costs for diagnosis and treatment. Despite the available arsenal of drugs and updated methods of etiopathogenetic treatment, POAG still remains unpredictable and is one of the main causes of incurable blindness.

Cortexin is classified as a direct neuroprotector. It reduces the intensity of free radical oxidation, has an antioxidant effect on nervous tissue, and has neuroprotective and anti-apoptotic effects. In addition, data have been obtained on its effect on restoring the autoregulatory ability of cerebral blood flow and improving ocular hemodynamics.

Cortexin is a complex of peptides isolated from the cerebral cortex of cattle. Cortexin contains amino acids, vitamins and microelements. The amino acid composition is represented by left-handed molecular structures, which increases the bioavailability of the drug.

Microelements (manganese, selenium, copper, zinc, etc.) included in the drug are involved in the regulation of apoptosis and support the activity of intracellular proteins and enzymes. The mechanism of action of Cortexin is associated with its metabolic activity: the drug regulates the ratio of inhibitory and excitatory amino acids, the level of serotonin and dopamine, has antioxidant properties, and reduces the level of anti-inflammatory cytokine TNF-α in the blood serum.

It is known that as optic nerve atrophy increases, dystrophic changes in the retina progress. According to Moshetova L.K. et al. retinal pathology in POAG is detected in 42.3% of cases. As a preventive therapy for dystrophic changes in the retina, the optimal combination of essential antioxidant vitamins (vitamins C and E), minerals (zinc and selenium), lutein and zeaxanthin - Okuwite Complete - is currently widely used.

To evaluate the effectiveness of using combinations of neuroprotectors with different mechanisms of action in the treatment of primary open-angle glaucoma (POAG) with compensated intraocular pressure.

MATERIAL AND METHODS

74 people were examined. (145 eyes) aged from 49 to 64 years (average 57.3±0.9) with stages I and II of POAG.

The initial stage of glaucoma was recorded in 28 people. (46 eyes), developed - in 32 people. (53 eyes), according to the classification of A.P. Nesterova. Glaucoma history is on average 4.9±0.8 years. There were equal numbers of men and women, all comparable in somatic status.

The condition for inclusion in the study was that the target IOP had been achieved with both medical and surgical treatment in history. All patients did not receive neuroprotective treatment for 6 months. (including drugs Brimonal, Betaxolol, etc. with a proven neuroprotective effect).

Exclusion criteria were severe lens opacity, severe macular degeneration, vascular diseases of the retina and optic nerve, diabetic retinopathy, a high degree of refractive error, severe somatic pathology, and uncompensated ophthalmotonus.

Patients of the 2nd group - 25 people. (50 eyes) received traditional therapy: emoxipine 1% -1.0 p/b - 10 days, then a month later in the form of instillations of 1 drop 4 times every 10 minutes - 20 days: vitamins B1, B6 - every other day 1.0 i/m; Aevit capsule in the morning after meals - 10 days; Thiocetam 1 tablet 3 times a day 30 minutes before meals - 30 days (repeat after 3 months).

Group 3 included 21 patients (40 eyes) who received only local antihypertensive therapy in the form of instillations.

All observed patients underwent visometry with best correction (BC), biomicroscopy, gonioscopy, computer perimetry on a Humphrey visual field analyzer (HFA II 740), tonography, fundus examination with a VOLK 78D lens, determination of the electrical sensitivity threshold (ESTH) and optic nerve lability by phosphene (critical frequency of disappearance of flickers by phosphene - CCIMF), optical coherence tomography (OCT), patient adherence to treatment was monitored. The presence of side effects, the patient's compliance with the instillation regimen, and changes in the patient's self-assessment of his condition and mood were clarified. Patients were observed for 6 months.

It is known that VA in glaucomatous optic neuropathy is not an objective indicator of the course of GON, but nevertheless significantly affects the patient’s quality of life. Subjective improvement in visual acuity was shown by 20 patients (40 eyes - 72.7%) from the first group of the study, 12 (24 eyes - 48%) - in the second group of the study, and in the third group by 5 patients (9 eyes - 22.5% ) a decrease in visual acuity was noted (Table 2).

There were no statistically significant deviations in morphological parameters according to OST data in patients of groups 1 and 2; in the control group there was a tendency towards a decrease in the layer of nerve fibers. At all stages of the study, good local and systemic tolerability of the drugs was observed.

CONCLUSION

Table 5 Average deviation of retinal light sensitivity in the central zone (MD), dB

Ivanova Nanuli Viktorovna - Doctor of Medical Sciences, Professor, Head. Department of Ophthalmology, State Institution “Crimean State Medical University named after. S.I. Georgievsky."

Galina Ivanovna Kondratyuk - assistant at the Department of Ophthalmology, State Institution "Crimean State Medical University named after. S.I. Georgievsky."

Dergalo Irina Ivanova - Candidate of Medical Sciences, Associate Professor of the Department of Ophthalmology of the Crimean State Medical University named after. S.I. Georgievsky."

Table 1 Distribution of patients by glaucoma stage and study groups

Table 2 Dynamics of corrected visual acuity (VA) in patients by study groups

In the pathogenesis of optical neuropathy, which is the cause of decreased visual function in glaucoma, along with mechanical and vascular factors, a significant role is played by metabolic reactions and apoptosis of retinal ganglion cells.

In this regard, special attention is currently paid to neuroprotective therapy in the treatment of glaucoma. Neuroprotection is understood as the protection of retinal neurons and nerve fibers of the optic nerve (i.e., retinal ganglion cells and their axons) from the damaging effects of various factors, as well as the normalization of neuronal-glial interaction and stimulation of macroglial cells to protect neurons from the toxic effects of glutamate and other pathological agents.

Neuroprotection is most effective only if intraocular pressure (IOP) is reduced to the level of “target pressure”.

Traditionally, treatment regimens for glaucomatous optic neuropathy include B vitamins. As a means of metabolic therapy, they stimulate adaptive-compensatory mechanisms, weaken the severity of various pathological processes, such as hypoxia, inflammation, lipid peroxidation, etc. The neurotrophic, antioxidant, regenerative, neuromodulatory, anti-sclerotic, immunostimulating, anti-stress effects of B vitamins are very important for ophthalmologists. As well as their participation in all types of metabolism, myelin synthesis, reducing homocysteine ​​levels, preventing NO inhibition and other effects that justify the advisability of using vitamins group B in the treatment of diseases of the optic nerve.

Many researchers still pay attention to the issue of using B vitamins in the complex treatment of glaucoma. So Panchenko N.V. et al. note the positive dynamics of electrical sensitivity and lability of the visual analyzer. Asregadoo E R. determined that the level of thiamine in the blood of patients with POAG is significantly lower than that of the control group. Yakovlev A.A. and Konde L.E. reported improvement in visual function in glaucoma patients using Riboxin. McCarty M.F. indicates the hypotensive effect of pyridoxine (due to its modulating effect on serotonin production). Kathleen Head notes stabilization of glaucoma over 5 years when taking vitamin B12 (without deterioration of visual fields, but also without effect on IOP).

TARGET

Table 3 Electrical sensitivity threshold for phosphene (ESTH) (μA) in the studied patients with POAG

Table 4 Critical frequency of disappearance of flicker by phosphene (CCIF) (Hz) in the examined patients with POAG

All patients were divided into 3 groups.

Group 1 - 28 patients (55 eyes) received combination therapy in the complex treatment of glaucoma: Cortexin IM 10 mg - 10 days (repeat after 3 months), Neurovitan 1 tablet 3 times a day - 1 month. Oxibral 1 capsule 2 times a day - 1 month. and Okuwait complete, 1 capsule 2 times a day with meals - 6 months.

The distribution of patients by stage of glaucoma in each group is presented in Table. 1. The groups of patients were comparable in terms of POAG stages.

RESULTS

The change in the electrical sensitivity threshold for phosphene (μA) in the studied patients with POAG is presented in Table. 3. It was found that the results were distributed as follows: 1st group - decrease in PAEF by 21.3%, 2nd - by 7.6%, control - increase by 6.6% (p<0,05).

The following anamnestic fact is noteworthy: if the first drug prescribed were drops from the group of prostaglandin analogues, PECP was always lower than that of others, which is obviously associated with a faster achievement of the target pressure and preservation of the electrical sensitivity of the nerve fibers. We found higher efficiency in terms of PECP in patients with POAG of group 1 when treated with combination therapy in complex treatment with a shorter glaucomatous experience.

At the same time, the increase in CCIMF in the 1st and 2nd groups was 13.4 and 3.9%, respectively, compared with the norm taken as 100%, with a decrease in the indicator in the control group by 3.4% (p<0,05) (табл. 4).

According to computer static perimetry (Table 5), there was an increase in the photosensitivity of the retina, more in group 1, a decrease in the number, area and depth of scotomas, an expansion of the area with normal photosensitivity.

In patients of the 1st group, there was a decrease in the size and depth of paracentral scotomas with an increase in MD by 16.4%, the same figure in the second group was 7.0%, and in the third group there was a deterioration in the indicator by 11.5% (Table 5).

The lack of positive dynamics in the control group of patients and significant improvement in visual functions when using various treatment regimens necessitates neuroprotective therapy.

Stabilization of neurodegenerative processes and improvement of the functional activity of the visual analyzer were obtained using a pathogenetically based combination of neuropeptides, vitamins, antioxidants and nootropic drugs. In this group, patients also noted an improvement in general well-being, increased attention and overall performance.

It is advisable to repeat courses of treatment once every 6 months.

Usmanova Asie Salimovna - ophthalmologist at city hospital No. 4

GLAUCOMA is an eye disease that occurs with increased intraocular

pressure and, if untreated, leads to blindness due to atrophy

optic nerve. The disease is progressive in nature and manifests itself in

mainly narrowing of the visual fields against the background of increased intraocular pressure. Symptoms of the disease are not noticeable to the patient and therefore require active detection.

Patients with open-angle glaucoma are strictly prohibited from:

Prolonged bending of the head down (laundry, mopping, working in the garden),

Lifting weights weighing more than 7 kg (weightlifting, heavy physical labor),

Sleeping on your stomach, face down,

Straining (constipation),

Compression of neck veins (tight collars, ties),

Overheating (long stay in a hot bath or sauna),

Consumption of excess fluid (no more than 1.5 liters per day) and table salt,

Overeating (stomach distension).

Prolonged coughing attacks are also undesirable and must be prevented with

medications. Patients with prostate adenoma should avoid straining when urinating.

Patients with NARROW-ANGLE GLAUCOMA are contraindicated from staying in the dark for long periods of time with their eyes open (insomnia), as well as taking medications that dilate the pupil (for example, used in the treatment of gastric ulcers).

High headboard when sleeping

Regular split meals (at least 5-6 times a day),

Breathing exercises,

Warming the extremities (hot baths for legs and arms in the absence of varicose veins),

Skin massage (warming),

Body weight control,

Prevention of colds,

Quitting or limiting smoking, limiting the intake of alcoholic beverages.

Treatment for glaucoma is aimed at reducing intraocular pressure and improving nutrition of the retina and optic nerve. To reduce intraocular pressure, antihypertensive drugs are used in the form of eye drops, which are prescribed individually by the attending physician. Instillation of drops should be regular in accordance with the regimen selected by the doctor. If necessary, treatment can be surgical.

Conservative treatment that supports the nutrition of the optic nerve and retina should be carried out regularly throughout the patient’s life, 2-3 courses per year, including the following drugs (as recommended by the attending physician) under the control of blood pressure:

Vasodilators and improve blood microcirculation (trental, nikoshpan, cinnarizine, cavinton, aescusan, etc.),

Improving metabolic processes in the retina and optic nerve (piracetam, photil, vitamins A, E, C and B).

Treatment should be coordinated with doctors of other specialties (therapists, neurologists, endocrinologists).

It should be remembered that it is undesirable to allow blood pressure to drop below the working level (in most cases 130-140 mm Hg) and rise above 160 mm Hg, since a sharp deterioration in the blood supply to the optic nerve and retina is possible.

The diet for glaucoma should be hypocholesterol, mainly plant-based, which is necessary for the collection of essential substances, including natural plant enzymes, as well as for the prevention of constipation. Sharp, spicy, salty foods that can cause thirst and lead to impaired water intake are excluded.

Intraocular pressure should be monitored at least once every 3 months, and visual fields should be monitored at least once every 6 months.

GLAUCOMA is a disease with a hereditary predisposition, so blood relatives of people suffering from glaucoma need regular preventive examinations over the age of 40 in order to early detect the disease.

For patients who have undergone SURGICAL TREATMENT for glaucoma, prescriptions are indicated individually by the attending physician in the discharge summary. It should be remembered that in the postoperative period it is necessary to observe a protective regime and limit physical exercise for 1 month. The regimen for instilling drops into the unoperated eye remains unchanged unless there are additional instructions from the attending physician.

REMEMBER! Success in the treatment of glaucoma depends on the efforts of not only the doctor, but primarily on the patient!!!

Ophthalmologist Gladkov V.L.

N.I.KURYSHEVA, Doctor of Medical Sciences, Professor, IPK FMBA of Russia, Moscow

Secondary neuroprotection

FOR GLAUCOMA

For many years, antihypertensive treatment of glaucoma has been the main therapeutic strategy. However, recently, due to changing ideas about the essence of the disease and its pathogenesis, neuroprotective therapy for glaucoma has become increasingly important, which in the coming years may become a fundamental method in the treatment of this serious disease.

In connection with neuroprotection, it is customary to distinguish between both the direct neuroprotective effect of a particular drug and its indirect effect (Levin L., 1999). In turn, direct neuroprotectors are divided into primary and secondary.

Primary neuroprotectors have a direct neuroprotective effect, the action of which is aimed at interrupting the earliest processes of the ischemic cascade: drugs that block NMDA receptors - remacemide, magnesia, lubeluzole, glycine, eliprodil, flupirtine, memantine and antagonists of voltage-dependent calcium channels.

Secondary neuroprotectors also have a direct neuroprotective effect, but their action is aimed at interrupting delayed mechanisms of neuronal death.

Considering the fact that neuroprotective treatment of glaucomatous optic neuropathy (GON) should be of a course nature and prescribed to a patient with glaucoma constantly, drugs that have no contraindications and can act preventively are more indicated for the treatment of GON. In this aspect, agents related to secondary neuroprotectors are preferable. Of these, the most promising is the use of peptide bioregulators, antioxidants and neuropeptides.

■ USE OF PEPTIDE BIOREGULATORS IN THE TREATMENT OF GUS

Significant optimism in the problem of neuroprotective treatment of glaucoma is due to the emergence of drugs called cytomedins, or peptide bioregulators. The term “cytomedines” was proposed by V.G. Morozov and V.H. Khavinson in 1983. It is derived from the Greek word “citos” and the Latin word “mediator”. Cytomedines obtained from various tissues using the acid extraction method have the ability to induce differentiation in the population of cells that are the starting material for their production. Those. after exogenous administration of these polypeptides, endogenous peptides are released, for which the introduced peptide was an inducer.

Cytomedins affect cellular and humoral immunity, LPO, and increase the body's defense reactions, regardless of what organs and tissues they were obtained from. Cytomedins, obtained from brain and retinal tissue, have the function of neuropeptides; they are actively involved in the regulation of the activity of nervous tissue. Currently, domestic drugs such as retinalamin and cortexin are widely used in ophthalmology.

Cortexin is a complex of peptides isolated from the cerebral cortex of cattle and pigs. Cortexin has a tropic effect on the cerebral cortex and regulates metabolic processes in the cerebral cortex, optic nerve and retinal neurons. The effectiveness of the drug in the treatment of GON, especially when used in the form of endonasal electrophoresis, was demonstrated in the recent work of L.A. Sukhareva et al. (2008).

It is impossible not to note the high effectiveness of Cortexin in the treatment of acute and chronic cerebrovascular accidents, its clear superiority over other neuroprotectors in the treatment of brain lesions in newborns, which is explained by

minimum course dose of the drug (only 0.2 g for 10 days of treatment), absence of side effects and affordable economic component of treatment. The experience of domestic medicine in this direction is represented by hundreds of works performed in recent years.

Retinalamine is isolated from bovine retina. It reduces destructive processes in the retinal pigment epithelium, improves the functional interaction of the pigment epithelium and the outer segments of photoreceptors. At present, the properties of retinalamine have already been studied experimentally and its effectiveness has been shown in diseases such as diabetic retinopathy, retinal vein thrombosis, pigmentary abiotrophy, and involutional central dystrophy. In 2002, at the Department of Ophthalmology of the Russian State Medical University of Moscow, together with Geropharm LLC (St. Petersburg), studies were carried out and the results of the therapeutic effectiveness of the drug retinalamin were published in patients with glaucoma with compensated ophthalmotonus (Nalobnova Yu.V. et al., 2003, 2004 ).

Employees of the Glaucoma Department of the Helmholtz Moscow Research Institute of GB conducted a comparative study of the effectiveness of peptide bioregulators in the treatment of patients with POAG (Erichev V.P. et al., 2005). The authors concluded that intramuscular and local administration of retinalamine and intramuscular administration of cortexin can be considered the most effective. It should be noted that improvements in retinal light sensitivity and contrast sensitivity were sometimes observed only 3 months after the end of the course of treatment, and mainly in patients with initial and advanced stages of glaucoma.

T.V. Stavitskaya and E.A. Egorov (2004) performed a comparative study of the neuroprotectors discussed above under conditions of experimental prolonged ischemia. The authors conducted electrophysiological studies (recording ERG and visual evoked potentials of the brain) while treating experimental animals with betaxolol, emoxypine, histochrome, cytochrome C and retinalamine. In addition, a morphological analysis of the retina of experimental animals was performed, including the study of ganglion neurons. As a result, high neuroprotective activity of betaxolol, retinalamine and emoxypine was discovered. It is noteworthy that during treatment with retinalamine, a repeated peak in the increase in electrophysiological parameters was observed with a new administration of retinalamine at a time exceeding the average time of retention of the drug in the retina, which is due to the activation of the retina’s own protective mechanisms during the use of retinalamine.

■ USE OF ANTIOXIDANTS IN THE TREATMENT OF GUS

To correct metabolism, antioxidants are used (emoxypin, mexidol, ascorbic acid, histochrome, vitamin E, rutin, drugs based on superoxide dismutase, quercetin). These drugs have antiaggregation and angioprotective properties and reduce the permeability of the vascular wall, viscosity and blood clotting, enhance the process of fibrinolysis, improve microcirculation, protect the retina from the damaging effects of light, and promote the resorption of intraocular hemorrhages.

Lutein complex has antioxidant properties. Thanks to the flavonoids included in the drug, vitamin A, beta

carotene, zinc and copper, the drug improves microcirculation in the retina, as well as tissue metabolism and promotes the regeneration of damaged tissue. Use of lutein complex 1 tablet. 2 times a day for 2 months showed the effectiveness of this drug in the treatment of GON (Moshetova L.K., 2005).

■ USE OF DRUGS INHIBITING APOPTOSIS

Establishing control over the processes of apoptosis is one of the most important strategic tasks of neuroprotection (T. Koike, 1991). The development of methods for anti-apoptotic protection of neurons under ischemic conditions has now begun.

The problem of drug suppression of apoptosis is due to the fact that apoptosis itself is a very significant mechanism in a physiological sense. When the balance of pro-apoptotic and anti-apoptotic factors is disturbed, breakdowns occur, leading to the development of severe cancer or degenerative diseases. By preventing apoptosis of retinal ganglion cells, we risk causing cancer. This can be illustrated by the administration of the anti-apoptotic agent bcL2, which is also a carcinogen, discussed in the literature (A. Bron, 2000).

Based on the achievements of modern molecular genetic research, laboratory synthesis of analogues of endogenous neurotrophins is carried out, turning off the mechanisms of “programmed” cell death. Of course, the results of this scientific search are of great interest and may determine future therapeutic strategies.

■ USE OF NO-SYNTHASE INHIBITORS IN THE TREATMENT OF GONNA

Nitric oxide release and peroxynitrite formation can be inhibited by nitric oxide synthase (NOS) blockers. The use of a selective blocker of neuronal NO synthase, 7-nitronindazole and 1-(2-fluoromethylphenyl)-imidazole, confirmed the effectiveness of this treatment in the clinic of ischemic brain lesions. Relatively selective blockade of inducible NO synthase (iNOS) by aminoguanidines also has a powerful neuroprotective effect. This drug was proposed as a neuroprotector in the treatment of GON by A. NeufeLd in 2004. From the standpoint of the currently recognized important role of NO in the pathogenesis of GON, this direction of neuroprotective treatment of glaucoma seems promising, but requires clarification, since the level of nitric oxide production changes as the disease progresses (Kurysheva N.I. et al., 2001).

APPLICATION OF PRODUCTS THAT IMPROVE

■ NEUROTROPHIC SUPPORT OF NERVOUS TISSUE

Neuropeptides play an important role in the functioning of nervous tissue. Neuropeptides work only “in the right place” and “at the right time” and then quickly disappear. The endogenous formation of a neuropeptide in response to any change in the internal environment leads to the release of a number of other peptides, for which the first is an inducer. This enhances and prolongs the effect of neuro-peptides.

Examples of drugs in this group are Cerebrolysin, Se-max, which is capable of regulating the expression of neurotrophins 3,4,5 and BDNF and has proven itself in the treatment of GON (N.I. Kurysheva et al., 2001).

Secondary neuroprotectors also include agents that improve ocular hemodynamics (aspirin, chimes, ticlid, trental, etc.), incl. and antagonists of the renin-angiotensin system rami-pril, captopril, which improve the visual fields of patients with glaucoma and reduce IOP when taken orally (Constad W., 1988; CostagLioLa C., 1995; Rekik R., 2002).

Ginkgo biloba has a polymorphism of effects, which is a trap for free radicals, including nitric oxide (Lugasi A., 1999), and also inhibits its production (Kobuchi H., 1997), reduces vasospasm of cerebral vessels, protects photoreceptors and retinal ganglion cells (GCS) from light damage, as well as suppressing the toxic effect of glutamate (Zhu I. et al., 1997). The drug improves regional blood flow in ischemic tissues and reduces the permeability of the capillary wall. To date, the effectiveness of treating glaucoma patients with this drug has been proven (Ritch R., 2000). To achieve a therapeutic effect, ginkgo biloba should be taken for a long time (at least 3 months).

■ IMMUNOLOGICAL ASPECTS OF GUS TREATMENT

Currently, data have been accumulated on the immune mechanisms of glaucomatous damage, as well as on the role of neuroglia in these mechanisms. BakaLash S. (2003) proposed using a kind of vaccination for neuroprotective purposes, in which the neuroglia itself acts as the antigen, and the resulting antibodies protect ganglion cells from pathological glial effects.

It has recently been established that a certain amyloid-beta protein is responsible for the apoptosis of RGCs, and in this regard, glaucoma is akin to Alzheimer's disease. Using a model of experimental glaucoma, it was shown that the use of antibodies to this protein can significantly reduce RGC apoptosis (Guo L. et al., 2007).

The literature discusses the possibility of using other neuroprotectors in glaucoma, such as cannabinoids, gangliosides, and statins. The use of the latter can be effective in reducing the risk of developing glaucoma, especially in people suffering from atherosclerosis (McGwin G., 2004).

Most secondary neuroprotectors also have reparative properties. All neurotrophic factors, modulators of the state of membranes and receptors (gangliosides), endogenous regulators (neuropeptides) have a powerful effect on the course of restoration processes in nervous tissue. At the same time, “primarily reparative” agents may also have some neuroprotective effect. Reparative drugs include nootropics - piracetam, picamilon, citicoline.

Perhaps the latest and most promising direction in the development of research in the field of neuroprotection should be considered the use of nanotechnology. This applies to both stem cell transplantation and the use of nanofibers, which provide regeneration of damaged axons (ELLis-Behnke R., 2006), and modulation of the work of ion channels located on neuronal membranes (Kramer K. et al. (2007).

In conclusion, it can be noted that modern understanding of the subtle mechanisms of development of glaucomatous optic neuropathy and rich experience in the use of neuroprotectors in neurological diseases with similar pathogenesis open up broad prospects in the scientific search for new ways of neuroprotective treatment of GON. The successes already achieved in this direction allow us to hope that neuroprotection will take its rightful place in the everyday treatment of primary glaucoma.

LITERATURE

1. Kurysheva N.I., Shpak A.A., Ioileva E.E. "Semax" in the treatment of glaucomatous optic neuropathy in patients with normalized ophthalmic tone // Vestn. ophthalmology. - 2001. No. 4. - P. 5-8.

2. Morozov V.G., Khavinson V.Kh. A new class of biological regulators of multicellular cytomedin systems // Advances in modern biology. - 1983. - Issue. 3. - P. 339.

3. Stavitskaya T.V., Egorov E.A. Study of the influence of neuroprotective drugs on electrophysiological parameters in conditions of prolonged ischemia // IY All-Russian School of Ophthalmology. - M., 2005. - P.324-332.

4. Ellis-Behnke R., Liang Y., You S., Tay D. Nano neuro knitting: peptide nanoflber scaffold for brain repair and axon regeneration with functional return of vision // Proc. Natl. Acad Sci USA. - 2006. - Vol.103. - P.5054 - 5059.

5. Levin LA. Retinal ganglion cells and neuroprotection for glaucoma //Surv. Ophthalmol. - 2003. - Vol. 48. - P. 21-24.