[The effect of sodium valproate on the electrical stability of the heart in experimental myocardial infarct]. / Vliianie natriia val'proata na élektricheskuiu stabil'nost' serdtsa pri éksperimental'nom infarkte miokarda.

It was shown in experiments on rats that sodium valproate, an activator of the stress limiting GABAergic system, prevents drop of cardiac fibrillation electric threshold in experimental myocardial infarction and restricts the development of extra-systole occurring in stimulation of the vagus nerve in rats with myocardial infarction. The possible mechanism of this effect is discussed.

[Elimination of disorders in the electrical stability of the heart during postinfarct cardiosclerosis by using a factor that induces GABA accumulation in the brain]. / Ustranenie narushenii élektricheskoi stabil'nosti serdtsa pri postinfarktnom kardioskleroze s pomoshch'iu faktora, vyzyvaiushchego nakoplenie GAMK v golovnom mozge.

It was shown that disturbances of the heart electrical stability in postinfarction cardiosclerosis manifested in a fall of the electrical threshold of the heart fibrillation and the development of extrasystoles during the vagus stimulation. These disturbances were effectively eliminated by administration of GABA in the brain.

[Prevention of arrhythmia in acute ischemia in conscious animals using a serotonin analog]. / Preduprezhdenie aritmii pri ostroi ishemii u bodrstvuiushchikh zhivotnykh s pomoshch'iu analoga serotonina.

The state of the serotonergic system was studied in adaptation of rats to short-term non-damaging stress actions along with the possibility of protecting the heart of conscious animals against arrhythmias in acute ischemia with the serotonin analogue 4-nitro-5-methoxytryptamine. It was shown that the adaptation resulted in a significant increase in rat midbrain serotonin by 70%. Preliminary administration of the serotonin analogue 3 fold reduced the total duration of arrhythmias and approximately 5 fold--the heart fibrillation rate and the death rate of animals in acute ischemia. The data obtained are in agreement with the idea on the role of stress-limiting systems in prevention of stress-induced and ischemic damages of the organism. They show that protective effects of metabolites of these systems can be successfully reproduced with their synthetic analogues or activators.

[Prevention of arrhythmias and cardiac fibrillation in acute ischemia and reperfusion by using a factor causing GABA accumulation in the brain]. / Preduprezhdenie aritmii i fibrilliatsii serdtsa pri ostroi ishemii i reperfuzii s pomoshch'iu faktora, vyzyvaiushchego nakoplenie GAMK v golovnom mozge.

Anticonvulsant sodium valproate, an inhibitor of GABA transaminase, which induces GABA accumulation in the brain, has been shown to possess a potent antiarrhythmic effect. In acute ischemia and reperfusion in conscious rats with closed chest, it decreased fourfold total duration of arrhythmias, while in nonanesthetized animals with open chest, it substantially limited the heart electrical fibrillation threshold and reduced fourfold total duration of arrhythmias. In both experimental models, sodium valproate decreased threefold the rate of ischemia-induced heart fibrillations. Clinicophysiological evaluation of the effect of sodium valproate on arrhythmias in coronary patients appears warranted.

[Prevention of a disorder in the electrical stability of the heart in experimental myocardial infarct by using preliminary adaptation to brief stress exposures and the antioxidant ionol]. / Preduprezhdenie narusheniia élektricheskoi stabil'nosti serdtsa pri éksperimental'nom infarkte miokarde s pomoshch'iu predvaritel'noi adaptatsii k korotkim stressovym vozdeistviiam i antioksidanta ionola.

Preliminary adaptation to short-term stress was shown to prevent the fall of the heart fibrillation threshold and its increased ectopic activity which is usually observed in experimental myocardial infarction. This protective effect involves an enhanced activity of the organism's antioxidant systems. On this basis, synthetic antioxidant ionol was applied to prevent disturbances of heart electric stability in infarction. Ionol completely prevented the decrease in the electric threshold and the increase in ectopic activity of the heart in experimental infarction, demonstrating thereby an anti-arrhythmic effect.

[Prevention of cardiac fibrillation using antioxidants and preliminary adaptation of animals to the effects of stress]. / Preduprezhdenie fibrilliatsii serdtsa s pomoshch'iu antioksidantov i predvaritel'noi adaptatsii zhivotnykh k stressovym vozdeistviiam.

Electrical ventricular fibrillation threshold (VFT) was determined, using programmed isolated stimuli on the left-ventricular apex, in male Wistar rats at different times after 10 hours' immobilization stress (IS). The VFT decrease reached a maximum of 48% 12 hours after IS. Cardiac sensitivity to the inhibiting vagal influence was increased considerably at the same time. The adaptation to short episodes of IS over 6 days, intermittent exposure to high-altitude hypoxia (5 hours daily at a 5000 m "altitude" for 40 days) and the antioxidant ionol (50 mg/kg) prevented IS-induced fibrillation threshold decrease. In cases of coronary arterial ligation in waking animals, the antioxidant ionol reduced fourfold the mortality associated with ventricular fibrillation and raised the spontaneous defibrillation rate from 28% to 72%. Possible mechanisms of these phenomena are discussed.