[Pharmacological correction of neuronal damage in sensomotor zone of frontal cortex under conditions of experimental cerebral blood flow pathology].

The administration of thiotriazoline, emoxypine and magnelong (a combined glycine-magnesium preparation) to animals with acute cerebral circulatory insufficiency showed significant neuroprotective effect in both acute and late ischemic periods, as indicated by the indices of cell density and number and the characteristics of apoptic and destructed neurons approaching those in the group of intact rats. Pyracetam showed cerebroprotective effect only in late ischemic period. Magnelong exhibited the most significant neuroprotective effect, maintaining cell density on the intact control level and reducing the number of apoptotic and destructed neurons.

[The effect of sodium salicylate and phenobarbital on the anti-arrhythmia properties of novocainamide and acetylnovocainamide]. / Vliianie natriia salitsilata i fenobarbitala na antiaritmicheskie svoistva novokainamida i atsetilnovokainamida.

CaCl2 and aconitic models of arrhythmias were reproduced in experiments with rats. Sodium salicylate was found to decrease the preventive effect of ecetylnovocainamidum and increased the effect of novocainamidum on ECG changes. Sodium salicylate diminished the preventive effect of acetyl-novocainamidum by elevating myocardial Na+ concentrations, favoured the decrease in myocardial K+ levels, eliminated the preventive effects of novocainamide and acetylnovocainamide by altering myocardial energy metabolism in CaCl2-induced arrhythmia and improved the preventive effect of acetyl-novocainamide on these parameters in aconitic arrhythmia.

[The effect of metabolic agents on the antiarrhythmic activity of novocainamide and acetylnovocainamide]. / Vliianie metaboliticheskikh sredstv na antiaritmicheskuiu aktivnost' novokainamida i atsetilnovokainamida.

The effects of potassium malate and sodium succinate on the antiarrhythmic activity of novocainamide and acetylnovocainamide during modelling of chlor-calcium-induced arrhythmia as well as in disorders of cardiac rhythm during modelling of pituitrin-isadrine-induced myocardial infarction were studied. The metabolic agents were found to increase the effectiveness of acetylnovocainamide and the toxicity of novocainamide. To interpret the specific features of the mechanism of the anti-arrhythmic action of the compounds there was studied their ability to form complexes with components of biomembranes and ions of biometals.

[The anti-arrhythmia activity of quinazopyrine]. / Issledovanie antiaritmicheskoi aktivnosti khinazopirina.

The antiarrhythmic activity of quinasopirine was studied in the experiments on rats with the use of models of calcium chloride- and aconitine-induced arrhythmias, disorders of cardiac rhythm in myocardial infarction produced by isadrine and pituitrin and also in the experiments on cats in arrhythmias caused by electric stimulation of the myocardium, postinfarction and reperfusion arrhythmias. Quinasopirine exhibits the antiarrhythmic effect being superior to that of anapriline and novocainamide in arrhythmias induced by calcium chloride and aconitine. In other types of the cardiac rhythm disorder its activity is comparable with that of ethmosine, obsidane and cordarone. Quinasopirine reduces automatism and contractile function of the myocardium.

[The mechanism of action of riboxin]. / K mekhanizmu deistviia riboksina.

The effect of riboxin (100 mg/kg body weight) on different kinds of metabolism in the cardiac muscles of Wistar rats in norm and during experimental pituitrin-neoepinephrine-induced myocardial infarction was studied. Riboxin was found to stimulate anaerobic glycolysis with the hyperproduction of lactate and the formation of glucose deficiency and also to increase the rate of protein synthesis on polyribosomes. Administration of riboxin during the formation of myocardial infarction considerably hinders the pronounced character of its electrocardiographic and biochemical manifestations. Thus, in the ischemic cardiac muscle the pool of macroergic phosphates is preserved, glycolysis and adaptive protein synthesis are impaired to a lesser degree that probably underlies the cardioprotective effect of riboxin.

[Effect of quinazopyrine on the process of reparative regeneration]. / Vliianie khinazopirina na protsessy reparativnoi regeneratsii.

The effect of quinazopyrine on skin wound healing in rats was studied. Quinazopyrine was found to stimulate synthesis of nucleic acids, maturation of fibroblasts and to increase mechanical strength of the postoperative scar. This effect retains in animals with alloxan-induced diabetes. The wound-healing activity of quinazopyrine was higher than that of methyluracil, dimexide, pentoxyl, sodium nucleinate, potassium orotate and riboxine.

[Biological activity of the sum of the valepotriates isolated from Valeriana alliariifolia]. / Biologicheskaia aktivnost' summy valepotriatov, vydelennykh iz valeriany chesnochnikolistnoi.

The native sum of valepotriates isolated from Val. alliariifolia Adams which was named valiracyl is an agent of low toxicity and exerts a pronounced neurotropic effect. Valiracyl suppresses the orientation reflex of animals in an "open field", decreases a spontaneous and caffeine-stimulated motor activity, potentiates and prolongs the action of barbiturates, significantly reduces aggressiveness of animals, decreases sensitivity to the convulsant effects of corasol and thiosemicarbazide, produces the antihypoxic and mild myorelaxant actions. The neurotropic effects of valiracyl are related to increased level of the GABA inhibition mediator and decreased intensity of bioenergetic processes in the brain.