MINISTRY OF HEALTHCARETASHKENT MEDICAL ACADEMY

DEPARTMENT OF PHARMACOLOGY

THEME:Antidepressants. Psychostimulant drugs. Nootropic drugs.

Plan of lecture

1. Overview of the stages of anesthesia

2. General characteristics of narcosis

3. Indications of narcosis.

4. Classification of narcosis.

5. Pharmacodynamics, pharmacokinetics of narcosis.

The aim of the lecture:

•generate knowledge about•Antidepressants. Psychostimulant

drugs. Nootropic drugs.

Pedagogical objectives:

- To characterize the stages of Antidepressants

- To introduce the general notion of Antidepressants

- Explain the indications for use Antidepressants

- Describe the classification of Antidepressants

- To reveal features of pharmacodynamics, pharmacokinetics of Antidepressants

• Antidepressants are substances used to treat depression. They can be represented by the following groups. I. Means that suppress neuronal uptake of monoamines 1. Indiscriminate blocking the neuronal uptake of serotonin and norepinephrine Imipramine amitriptyline 2. Selective effect A. The blocking neuronal uptake of serotonin Fluoxetine B. blocking neuronal uptake of norepinephrine Maprotiline II. Monoamine oxidase (MAO) 1. Indiscriminate inhibitors (MAO-A and MAO-B) Nialamide transaminase 2. Of selective inhibitors (MAO-A), Moclobemide

• Very common in medical practice were the first group of drugs, which are tricyclic antidepressants ¬ Santa. They refer to antidepressants indiscriminate blocking reverse neuronal uptake and serotonin and norepinephrine. One of their representatives - imipramine (imipramine, imipramine, Tofranil). He has a pronounced anti-depressive properties, which ¬ cetana weak sedative effect. However, under certain conditions detected and psihostimuliruyuschy component (sometimes there is some agitation, euphoric, maybe insomnia). Regarding the mechanism of action of imipramine makes a number of assumptions ¬ tions. One of the most accepted hypothesis relates it antidepressant effect ¬ fect with the ability to inhibit neuronal uptake of norepinephrine and serotonin ¬ on.

• This leads to the fact that in the receptor accumulate high concentrations of neurotransmitters and their effects are magnified. In particular, strengthening ¬ tor strahlung effect of serotonin on the limbic system (the amygdala) mo ¬ may be an important mechanism of action of antidepressant imipramine. The drug also blocks the presynaptic a2-adrenergic receptors (which increases ¬ decreases the release of noradrenaline), serotonin (5HT | D t) and histamine receptors. Along with the central action of imipramine has some of peripheral ¬ kim m-anticholinergic (atropine), adrenoblokiruyuschim, papaverinopodobnym protivogistaminnym and distinct effects. From the gastro-intestinal tract is absorbed well imipramine.

• In a significant degree ¬ tion is metabolized in the liver. One of its metabolites - desmethyl-imipramine (desipramine) - has expressed antidepressant activity and is used in medical practice. Excreted as metabolites, conjugates and unchanged in the kidneys (40% - on the 1st day), partly intestine. When using imipramine in depression treatment effect occurs che ¬ cut 2-3 weeks. Side effects most often associated with atropine their properties ¬ imipramine (dryness of the mouth, disturbance of accommodation, tachycardia, constipation, difficulty in urination). Violations of the law and of the ser ¬ dechno cardiovascular system. Imipramine in therapeutic doses may reduce the ar ¬ ter pressure. So, against his actions sometimes develop orthostatic hypotension. In high doses can cause tachycardia, arrhythmias. Possible adverse deviation on the part of mental activity. This is either excessive sedation, or, on the contrary, the excitement, the Gallo ¬ tsinatsii, and insomnia. When receiving imipramine may be headache, tremor, allergic skin reactions, jaundice, leukopenia, and agranulocytosis is rare. Pres ¬ Parat also contributes to weight gain.

•Imipramine is contraindicated in glaucoma, urinary abuse associated with hypertrophy of the prostate. You can not combine it with indiscriminate ¬ tive MAO inhibitors, as this toxic effects occur ¬ you. If these two types of antidepressants prescribed sequence, the interval after discontinuation of MAO inhibitors should not be less than 1.5-2 weeks. Similar to a drug imipramine clomipramine (Anafranil). Lee Bo ¬ expression affects the reuptake of serotonin.

• Amitriptyline (triptizol) structurally similar to imipramine. Pharmacodynamics and pharmacokinetics of amitriptyline and imipramine are similar. In addition to the antidepressant activity of amitriptyline are expressed in psychosedative properties. The stimulatory effect of it available. In addition, it is superior to imipramine for m-anticholinergic and antihistaminic action. Amitriptyline is among the most active antidepressant ¬ by intense media. The therapeutic effect it is revealed in 10-14 days.

• It also includes tricyclic antidepressants azafen (pipofezinum). It has a mild antidepressant activity and has a sedative effect. Different in a positive way from those antidepressant lack of m-anticholinergic properties. Apply azafen with depression of mild to moderate severity. The drug was well tolerated. Side effects are observed only in certain cases, so azafen recom ¬ mended often elderly patients. Assign it inside. Reported drugs act indiscriminately on the neuronal uptake of serotonin and norepinephrine. However, drugs and created a voter ¬ nym action. Thus, the synthesized compounds, especially depressing neuronal uptake of serotonin. One such drug is fluoxetine (Prozac frameks). According to the chemical structure, it is derived phenoxypropylamino.

• . It has high anti-depressant activity, ana ¬ logical that for tricyclic antidepressants. The effect is at ¬ gradually (within 1-4 weeks). From tricyclic antidepressants is different in that it has virtually no sedation and is usually not detected ¬ inducing effect that no or only very slightly m-anticholinergic action, not marked effect on adrenergic receptors. Ge ¬ thermodynamics when fluoxetine is stable. Body weight does not increase ¬ is. Furthermore, fluoxetine has low toxicity. Well absorbed when administered inside. Metabolized in the liver. One of its metabolites, norfluoxetine, has a pronounced anti-depressant ac ¬ ciency. For fluoxetine, t 2 = 1-3 days (for norfluoxetine - 7-15 days). Stand metabolites and unchanged drug by the kidneys. Of the side effects observed violation of appetite, nausea, nervousness ¬ sion, headache, insomnia, skin rashes.

• You can not use fluoxetine with non-selective MAO inhibitors may develop as a so-called "serotonin syndrome" associated with the accumulation of excessive concentrations of serotonin. This may be the muscular rigidity, hy ¬ pertermiey and cardiovascular collapse, which is a danger to life. With that said between doses of fluoxetine and non-selective MAO inhibitors should be an interval of at least 2 weeks. Interactions with food ingredients for fluoxetine were observed (as opposed to non-selective MAO inhibitors.) Fluoxetine has been widely used in medical practice in the treatment of depressive states ¬ chenii. Selective inhibitors of neuronal uptake of serotonin for copper ¬ Qing practice offers a number of new drugs - setralin, paroxetine, etc. The highest selectivity of action has paroxetine (Paxil).

• ). In vitro experiments have shown that paroxetine 320 times stronger inhibits the reuptake of serotonin, norepinephrine than (setralin - 190 times fluokse ¬ ting - 20 times). Paroxetine has high anti-depressant and anxiolytic (anxiolytic) activity. Has little m-holinob ¬ lokiruyuschee deystvie.Pri enterally absorbed completely. 93-95% of the material ¬ Vaeth binding to plasma proteins. Most of paroxetine metabolized in the liver of active metabolites are formed. Metabolites are distinguished mainly by the kidneys (~ 62%), the rest of the intestine is derived, t ~ 21 hours time "semi ¬ life" of the drug increases with kidney failure and cirrhosis of the liver. 1 introduced the drug once a day. The effect develops within 1-4 weeks. Pro ¬ duration of treatment is measured in months, depending on the type of depression.

• Paroxetine is well tolerated. Side effects are rare. Nausea, headache, sometimes dryness in the mouth, drowsiness, dizziness, etc. Also synthesized drug that selectively blocks the neuronal norepinephrine doses ¬ vat - maprotiline (ludiomil). According to its pharmacological properties and ¬ to the application is similar to imipramine. Absorbed from the digestive tract slow (9-16 hours). About 90% of the drug binds to plasma proteins, t, = 43-51 hours Undergoes bio ¬ transformation in the liver. Distinguished maprotiline and its metabolites in the main ¬ nom kidneys.

•The predominant influence on the neuronal uptake of norepinephrine region ¬ also gives desipramine. As already noted, it is a metabolite of imipramine. By the nature of the action is similar to the last one. Causes less sedation and m-anticholinergic effects. Antidepressants of the group of MAO inhibitors are divided into non-selective drugs and selective action.

• Currently indiscriminate inhibitors of MAO (affects MAO-A and MAO-B) is used relatively infrequently due to the rather high toxicity. When choosing an antidepressant preference is usually given to drugs that affect her ¬ coronal monoamine uptake. However, in some cases, may be useful ¬ inhibition of MAO inhibitors, particularly selective. Non-selective MAO inhibitors inhibit the process of oxidative deamination of norepinephrine and serotonin, which leads to their accumulation in the brain tissue values ¬ considerable amount. The majority of this group of drugs block the irreversible MAO ¬ reversibly. In this regard, recovery MAO it must be synthesized anew, which requires considerable time (up to 2 weeks).

• ). Its maximal inhibition occurs several hours after the intake of MAO inhibitors. However, the antidepressant effect develops within 7-14 days. Apparently, the mechanism of action of this group of substances is associated not only with inhibition of MAO, as between this effect and the en ¬ tidepressivnoy activity is not always overlap. It is possible that the definition ¬ lennuyu role can the impact of these drugs on the exchange of GABA. Along with antidepressant MAO inhibitors are characterized by pronounced ¬ GOVERNMENTAL psycho-stimulant properties (cause euphoria, excitement, sleepless ¬ zu).

• MAO inhibitors are active antagonists of reserpine in relation to its sedative, hypotensive and other types of actions. This is due to the fact that the re ¬ zerpin lowers in the brain catecholamines and serotonin, and MAO inhibitors eye ¬ shows the opposite effect. Against the background of the action of MAO inhibitors dramatically enhanced pressor effect sympathetic-mimetics (amphetamine, ephedrine, tyramine), including in food pro ¬ product (for example, in the cheese, there are significant amounts of tyramine). These substances contribute to the release of adrenergic endings of excessive amounts of noradrenaline ¬ ling, which accumulates in them as a result of MAO inhibition. Thus there is a hyper-hypertensive crisis.

• Inhibition of MAO inhibitors are influenced by it occurs not only in the CNS but also in peripheral tissues. Furthermore, these drugs inhibit the activity of MAO not only, but also a number of other enzyme systems. Thus, due to inhibition of microsomal liver enzymes ¬ ments MAO inhibitors prolong the action means for neingalyatsionnyh anesthesia, antipsychotic phenothiazine series, opioid analgesics, anti-epileptic and other means. MAO inhibitors possess antihypertensive activity, which is apparently due to the decrease in the release of norepinephrine from varicose thickenings adrenergic ¬ FIR fibers. When they reduce angina pain (apparently due to block ¬ kirovaniya central parts of reflections with the heart). MAO inhibitors are absorbed from the digestive tract is good. Are distinguished primarily by the kidneys. MAO inhibitors have a relatively high toxicity. This is manifested mainly in respect of the liver (can cause severe hepatitis).

• Furthermore, they excite the CNS, which is the cause insomnia and in some cases resulting tremor and convulsions. The use of these agents may be accompanied by orthostatic hypotension. With the improper cau ¬ MAO inhibitors should be combined with other neurotropic agents ¬ mi, since it is often accompanied by adverse effects (eg, in combination with the type of action of narcotic substances, sympathomimetic, antidep ¬ ressantami tricyclic series). Furthermore, the reception MAO inhibitors should be deleted from the diet foods containing tyramine (cheese, etc.). Drug dependence in relation to MAO inhibitors does not develop.

• As MAO inhibitors have been synthesized derivatives of hydrazine. However, currently used in medical practice hydrazine single drugs such nialamide (niamid, nuredal). This is one of the least effective ¬ her antidepressants. However, toxic effects on the liver and its other side-effects are to a small extent, that is doubtless worthy ¬ stvom nialamidom. Another class of chemical compounds refers transaminase (tranylcypromine, parnat). It is phenylcyclopropylamine, i.e. similar in structure of phenylalkylamines (e.g. fenaminu). Transaminase - a strong reversible inhibitor of MAO. It belongs to the most effective antidepressants in this group. The therapeutic effect of it comes a little faster than most new hydrazine ¬ (at nialamidom - in 12-14 days, transaminase - in 2-7 days). Pharmacodynamics transaminase similar to that of other MAO inhibitors. To this should be added ¬ mu of its certain sympathomimetic effect (effect of amphetamine-type). Hepatotoxicity y "negidrazinovyh" compounds is less pronounced than in preparations of hydrazine.

•Antidepressants of indiscriminate group of MAO inhibitors are contraindicated in diseases of the liver, kidney, stroke, severe mental stimulation. In recent years attention of preparations advantageously reversible inhibitor of MAO-A. These include moclobemide (auroriks) pirazidol, etc. They are more briefly than the irreversible MAO inhibitors. In addition, when used reduces the risk of hypertensive crisis when interacting with sympathomimetic food prois ¬ walking (eg, tyramine), which is typical of non-selective MAO inhibitors ¬ tors. Moclobemide is a derivative of benzamide.

• Pirazidol - is a tetracyclic compound. The chemical structure, it can be referred to derivatives of indole. Pirazidola antidepressant effects, depending on the patient's condition is combined with a sedative (against the troubles are, anxiety) or challenging (in the face of oppression) effect. Fur ¬ mechanism of antidepressant action is explained by its inhibitory effect on the reversible MAO-A and the ability to inhibit neuronal uptake of norepinephrine. M-holinoblokiruyushaya activity in pirazidola missing. Transferred pre ¬ Parat well. Side effects are rare. Take pirazidol inside. Stimulants Stimulants increase the mood, ability to perceive beyond ¬ shnih irritations, psychomotor activity. They reduce the feeling of tired ¬ STI, enhance physical and mental performance (especially in fatigue) temporarily reduces the need for sleep.

•According to the chemical structure of •psychostimulants include the following groups.

Phenylalkylamines Benzedrine Piperidine derivatives Pipradol Merida Derivative sydnonimine Sidnokarb Methylxanthines Caffeine

• Is a typical stimulant amphetamine (amphetamine sulfate). It seems a pre ¬ fenilalkilamina ie similar in structure to adrenaline and noradrenaline. By fenaminu belongs entirely characteristic given to the whole group psihostimu ¬ liruyuschih substances. The mechanism of action of amphetamine exciting explain its ability to release from presynaptic terminals norepinephrine and dopamine. The released catecholamines stimulate the appropriate receptors are present in the CNS. In addition, amphetamine, apparently somewhat reduces neuronal uptake of noradrenaline and dopamine.

• A stimulating effect of amphetamine is attributable largely to its stimulant effect ¬ tion on the ascending activating reticular formation of the brain stem. This is manifested in the EEG desynchronization of bioelectrical activity. However, it is possible that amphetamine excites neurons of the cerebral cortex directly. Moreover, it stimulates the formation of specific inhibits limbic system and neo-striatum. On the development and implementation of conditioned reflexes amphetamine in small doses, has a beneficial effect, in large - oppresses them. In this case important is the type of nervous system. For amphetamine characterized its effect on food center, located in the hypothalamus ¬ Musa, which leads to the suppression of hunger.

• Amphetamine has a direct stimulatory effect on the respiratory center, which pro ¬ is mostly against his oppression. In this case, amphetamine acts as an analeptic. Phenamine not only acts on the CNS but also in peripheral nerve. It exerts an indirect stimulatory effect on the alpha-and beta-adrenergic receptors. ¬ As already mentioned, amphetamine refers to sympathomimetics (causes the release of noradrenaline ¬ Nalini thickening of varicose adrenergic fibers). It has a direct effect on adrenergic receptors, but it is of secondary importance. Sympathetic-and amphetamine Adrenomimeticalkie properties are largely in increasing arterial pressure ¬ tion. In this regard, amphetamine inferior in activity adrenaline 100-150 times but its pressor effect considerably prolonged. Effect on smooth muscle organs other similar adrenaline, but expressed to a small extent. From the digestive tract of the drug is absorbed well.

• . Quickly penetrates the blood-brain barrier. In the body, biotransformation an hour ¬ partially. Excreted by the kidneys in a large part (30-50%) as unchanged. To reduce its concentration in the blood plasma of 50% requires about 12 hours when the pH shifts toward acidic urine, excretion rate amphetamine increases.

With prolonged use of amphetamine accumulates, develop tolerance to it and drug abuse (physical and mental). Apply amphetamine mainly in neurotic subdepression, as well as narcolepsy and similar conditions involving sleepiness. Furthermore, it is sometimes used to improve performance in fatigue. In this case, it should be noted that the stimulating effect of amphetamine is accompanied by a large sam ¬ ratoy energy resources of the body, so after a good rest to recuperate absolutely necessary. Amphetamine is sometimes prescribed as a analeptic drug poisoning substances ¬ arithmetic type of action. To reduce the appetite amphetamine use is impractical because it causes excitement, raises blood pressure and is a poten ¬ tial dangerous drug with respect to the development of drug dependence.

• In case of overdose are marked agitation, anxiety, insomnia, tachycardia, a rhythm disturbance sometimes heart rate. Amphetamine contraindicated in aterosk ¬ leroze, hypertension, insomnia, in old age. Currently, amphetamine is rarely used (due to its ability to cause drug dependency). Fenaminu similar in their effect on the central nervous system, piperidine derivatives pipradol (pipradol) and meridil (methylphenidate hydrochloride, centedrine). By stimulating asset ¬ sion pipradol not inferior fenaminu. Meridia works less hard. The apparent advantage pipradol and Merida is the absence of unwanted peripheral ¬ toric Adrenomimeticalkie effects.

• In particular, unlike amphetamine prac ¬ cally they do not affect the cardiovascular system. Active psychoactive agent is also sidnokarb. According to the chemical structure it refers to the group sydnonimine. ¬ psychoactive effect extending sidnokarba develops gradually and persists for a long time ¬ mja. Euphoria and motor driving is not observed. Mechanism of action psychostimulant obviously associated with the activation of noradrenergic system. Compared with fenaminom sidnokarba have no pronounced peripheral sympathomimetic effect. This is evident in the relative ¬ but stable hemodynamics. Sidnokarb well tolerated. If overdose ¬ renormalization possible agitation, anxiety, insomnia, ¬ tion slight increase in blood pressure. In the evening hours sidnokarb should not be accepted, as it can disrupt sleep.

• The group also includes stimulants caffeine (the compound of the group ¬ Py methylxanthines). It is an alkaloid contained in leaves of tea (Thea sinensis), a in the seeds coffee (Coffea arabica), cocoa (Theobroma cacao), cola (Cola acuminata) in other plants. Caffeine combined analeptic and psychostimulant properties. Especially pronounced him a direct stimulating effect on the to ¬ py brain. Caffeine stimulates mental activity, enhances mental and physical performance, motor activity, ¬ reproach ourselves to the reaction. After receiving his vigor appears temporarily eliminate ¬ nyayutsya or decrease fatigue, drowsiness. The effect on the higher nervous activity largely depends on the type and dose of caffeine nervous system. In small doses of caffeine have dominated STI ¬ stimulating effect, in large - depressing. It should be borne in mind that for a weak type of nervous system excitation effect is achieved by introducing small amounts of caffeine, whereas for the strong type requires much pain ¬ Chiyah dose.

• Analeptic activity is associated with the effect of caffeine on the continued ¬ govatogo centers of the brain. It has a direct stimulatory effect on the respiratory and vasomotor centers. There are quickening and deepening the breath, which is particularly evident at the center of the oppression of breathing. In addition, to ¬ Fein exciting centers of the vagus nerves. On the spinal cord ¬ drug action exists only in high doses. By facilitating the transfer of impact interneural ¬ tation it enhances the spinal reflexes. Significant place in the pharmacodynamics of caffeine is its impact on the mid ¬ dechno-vascular system. It consists of the peripheral and central effects. For example, caffeine has a direct stimulatory effect on the myocardium. However, at the same time excited centers of the vagus nerves, so to ¬ finite effect depends on the prevalence of a particular influence. Usually measured in ¬ tion of the heart (if they occur at all) are small.

• In large doses, caffeine causes tachycardia (ie, dominated by its peripheral action of), sometimes arrhythmia. Central and peripheral components in the action of caffeine are in respect of vascular tone. By stimulating the vasomotor center, coffee ¬ Institute increases vascular tone, and the direct effects on vascular smooth muscle tone reduces them. Caffeine has an ambiguous effect on the various vascular regions. Thus, the coronary blood vessels dilate more often (especially if cardiac output is increased). However, some brain vessels toned. The latter apparently explains beneficial effect of caffeine in migraine. On the other ¬ Gia smooth muscle organs (bronchi, bile duct), caffeine has a mild ¬ tion myotropic antispasmodic effect on skeletal muscle - stimulating ¬ separating (central and direct). Even more difficult to change blood pressure, since it depends on kardiotropnyh and vascular effects of caffeine. Usually, if the initial partial pressure of arterial ¬ normal, caffeine does not change or only slightly by ¬ ceeding it.

• . If the drug is introduced against the background of hypotension, blood pressure increased (normalized). Caffeine increases the basal metabolic rate. Increases glycogenolysis, causing hy ¬ perglikemiyu. Increases lipolysis (free fatty acids in plasma ¬ IU increases). In large doses, causes the release of adrenaline from the brain ¬ traction adrenal medulla. Observed in the application of the central effects of caffeine, the effect on the smooth and striated muscle, changes in metabolism, some authors attributed to the accumulation of cAMP. There is it seems, partly in re ¬ result of phosphodiesterase inhibition and disturbances in connection with this process, consider ¬ decay of cAMP. In more caffeine inhibit phosphodiesterase brain and heart, but this occurs only at very high concentrations exceeding therapeutic. In recent years the accumulated data confirm maintainer, more important component of the action of methylxanthines (caffeine, theophylline) is their antagonism of adenosine. It is important to note that this is ¬ observed at therapeutic concentrations of methylxanthines.

• In favor of this view is evidenced by the fact that methylxanthines and adenosine cause pro ¬ oppositely directed effects. Furthermore, it was shown that the above effects of adenosine eliminated methylxanthines, which blocks ¬ sealing against adenosine A - and A2-receptors (are competitive antagonists ¬ Tammy adenosine). Under the influence of caffeine increased secretion of gastric glands, and may be used for diagnostic purposes. The use of caffeine in the pathology of the stomach (gastritis / ulcer, tumor) helps differentiate func ¬ ktsionalnye violations of organic.

• In a small degree of caffeine increases urine output, which is associated with inhibition of pro ¬ process of reabsorption in the proximal and distal renal tubular sodium and water. In addition, caffeine dilates blood vessels and increases renal fil ¬ tration in the renal glomeruli. Caffeine and especially its water-soluble salts are well absorbed from the intestine ¬ nick (including the colon). The main part of it is exposed biotransformation ¬ formation (demethylated, oxidized). About 10% of the caffeine is released by the kidneys unchanged. With prolonged use of caffeine develops Just noticeable pref ¬ circuiting. You may experience psychological dependence (theism). Caffeine is used to stimulate mental activity, when wearied, research institutes, migraine, hypotension. It is part of many combined preparations ¬ Ratov in combination with non-narcotic analgesics (pill "Citramon-P", etc.), and ergot alkaloids (pill "Kofetamin"). Side effects are manifested in the form of nausea, vomiting, restlessness, ¬ impact excitation, insomnia, tachycardia, cardiac arrhythmias. Caffeine is contraindicated in severe arterial hypertension, ateros ¬ sclerosis, sleep disorders, glaucoma.

•                                   Nootropics They have a direct activating effect on the integrative mechanisms of the brain, stimulate learning, improve memory and mental performance, increase the resistance of the brain to the "aggressive" actions. Improving the mental, mental activity is the main effect of this group of substances. This manifests itself in mental ¬ sufficiency not associated with organic brain damage. On the higher nervous system healthy animals and healthy human psyche, these drugs have no effect. So, normally they do not change many of the behavioral reactions, reflexes, brain bioelectrical activity, motor activity. At the heart of the action of pharmacotherapeutic nootropov in pa ¬ ontology is a beneficial effect on metabolism (energy) pro ¬ cesses of the brain. Key nootropic agents used in medical practice, mimic the metabolic effects of gamma-aminobutyric acid (GABA).

• Nootropics have a therapeutic effect with mental deficiency only long-term use, that is, they have the knowledge ¬ nificant latency in action. These preparations are used in some cases in combination with other psychotropic agents in the treatment of various psychiatric patients. Most of the known nootropics has also antigipoksicheskoy and anticonvulsant activity. The group includes Aminalon nootropics, piracetam, atsefen, etc. The most widely used Aminalon and piracetam. Aminalon (gammalon, genevrin, encephalon) is the drug of GABA in the central nervous system. GABA acts as a neurotransmitter braking and also plays an important role in the metabolic processes of nerve tissue. Last seen in the stimulation of tissue respiration (or GABA acts as a respiratory substrate or activating ¬ viruet enzymes of the Krebs cycle). Metabolic activity of GABA and lies at the heart of its psychotropic effect. The drug Aminalon obtained by synthesis. Aminalon reduces the manifestations of mental deficiency, ¬ necks arose in connection with a variety of chronic organic brain damage.

• The blood-brain barrier drug goes bad. However, with organic lesions of the brain permeability through aminalona n ¬ matoentsefalichesky barrier increases. Aminalona important properties are its ability to increase cerebral blood flow and oxygen tension in the tissues of the brain and the mind ¬ rennaya-hypoxic activity. In addition, Aminalon has anticonvulsant activity, which ¬ paradise is obviously connected with the normalization of the content of GABA in the brain and particularly in the epileptogenic foci. Aminalon causes a slight reduction in blood pressure with a bradycardia. The hypotensive effect is most pronounced on the background of hypertension. At a high content of sugar in the blood hypoglycemic effect. On the contrary, with a normal level of blood sugar Aminalon often leads to moderate hyperglycemia (associated with glycogenolysis). Used mostly with mental deficiency, caused ¬ tion ischemic attack (in atherosclerosis, stroke, trauma, skull, etc.), in alcoholic dementia and in mentally retarded children. Aminalon sometimes used in the treatment of epi ¬ Leps. You can also use the hypotensive action of the drug in the treatment of patients with arterial hypertension. The action of the drug develops gradually. The treatment continued ¬ is a few months. Enter the product inside and intravenously. Aminalon well tolerated. With prolonged use may diarrheal disorders, sleep disorders, sometimes - ¬ tial fluctuations in arterial pressure.

• Piracetam (Nootropil, Pyramus) is a cyclic derivative of GABA ¬ nym. Just as Aminalon has a beneficial stimulating ¬ ating effect on mental activity (thinking, learning, na ¬ crease). It facilitates the transfer of information between the hemispheres of the brain, stimulates the transfer of excitation in the central neurons, improves blood circulation and energy processes of the brain. An important property of piracetam is its anti-hypoxic effect. Stability of brain tissue to hypoxia on the increase. In addition, piracetam has an anticonvulsant effect, preventing dis ¬ gation of seizure activity. The mechanism of action of piracetam is poorly understood. The drug is similar to GABA and GABAergic agents. Piracetam easily penetrates through tissue barriers. Quickly suc ¬ Vaeth of the intestine passes through the blood-brain and placental barrier ¬. Stands out from the body primarily by the kidneys, but predominantly ¬ unchanged.

•Applied piracetam with mental deficiency associated with chronic vascular and degenerative lesions of the brain (in old age, atherosclerosis, by alcoholysis ¬ ma, cranial trauma, etc.). Pyracetam administered oral and parenteral one to several months. Of the side effects sometimes observed diarrheal rasstroyst ¬ va, sleep disorders. A contraindication is pregnancy, acute renal failure.

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