[Glucose consumption by the rat brain in ethanol intoxication and the abstinence syndrome]. / Potreblenie gliukozy golovnym mozgom krysy pri intoksikatsii étanolom i sindrome otmeny.

The effect of acute and chronic alcohol intoxication and of the syndrome of ethanol withdrawal on the consumption of glucose by the brain of rats was studied by means of intravascular ethanol infusion. Infusion of ethanol into the internal carotid artery had no effect on glucose consumption by the brain, while its infusion into the femoral vein reduced consumption twofold. The effect was completely removed by the inhibitor of alcohol dehydrogenase pyrazole. Chronic intoxication also caused a twofold decrease of glucose utilization by the brain of rats. Infusion of ethanol into the internal carotid artery of rats who were in a state of alcoholic intoxication led to increase of glucose consumption by the brain to the control level. Infusion of ethanol into the femoral vein in this case had no effect on glucose consumption by the rat brain. Utilization of glucose by the brain diminished to an equal degree in rats suffering from the syndrome of ethanol withdrawal and in animals who were in a state of alcoholic intoxication. Infusion of ethanol, both intraarterial and intravenous, had no effect on glucose consumption by the brain. Activation and inhibition of the function of external respiration were encountered in equal concentrations of ethanol in blood flowing from the brain, whatever the method of its infusion.

[The effect of insulin on lethality in mice with acute ethanol poisoning]. / Vliianie insulina na letal'nost' myshei pri ostroi intoksikatsii étanolom.

Intraperitoneal injection of 25% ethanol solution in LD80 doses caused death of approximately 60% of satiated and starving animals in the first 60 minutes. The death peak was encountered 3-10 minutes after the injection of ethanol and corresponded with the peak of its concentration in the blood. The early death of the animals was connected with arrest of respiration in inhibition of cardiac activity. A tendency towards increase of ethanol LD50 60 minutes after its injection in administration of insulin was encountered. The changes of ethanol LD50 were statistically insignificant.

[Cardiac effects of insulin in ethanol intoxication and in the postintoxication period]. / Kardial'nye éffekty insulina pri intoksikatsii étanolom i v postintoksikatsionnyi period.

Insulin (2 IU/ml) effect on the contractile function, glucose consumption and lactate release by the myocardium was studied in experiments on the isolated rat heart performed at different time after a single (8 g/kg) and 10-fold with a 12-hour interval (8-10 g/kg) intragastric administration of ethanol. A single administration of ethanol failed to influence the contractile function, glucose consumption and lactate release by the isolated heart. The magnitude of a positive inotropic reaction to insulin increased and its stimulating effect on glucose utilization by the myocardium weakened. The reaction of ethanol withdrawal developing after its 10-fold administration led to a disturbance of the contractile and rhythmic functions of the heart and activation of glycolysis. The heart inotropic reaction to insulin in this period weakened and glucose consumption and lactate release stimulated by insulin did not differ from control. During perfusion of intact rat hearts with and without glucose insulin (2 IU/ml) weakened the cardiodepressive effect of ethanol (200 mM).

[Contractile function, glucose consumption and lactate release by the isolated rat heart during different regimens of alcohol administration and after discontinuation of ethanol]. / Sokratitel'naia funktsiia, potreblenie gliukozy i vysvobozhdenie laktata izolirovannym serdtsem krys pri raznykh rezhimakh alkogolizatsii zhivotnykh i posle otmeny étanola.

Acute or chronic intoxication of rats with ethanol (intragastric administration at a dose of 8 g/kg or free-choice drinking of 10% ethanol for 3 months) produced no significant changes in contractile function, glycogen content, glucose uptake and lactate release in isolated hearts. Withdrawal syndrome simulated in rats following a short period of severe intoxication with ethanol at a dose of 4-5 g/kg twice daily has demonstrated a 15 and 28% decrease in peak systolic pressure and tension time index, respectively. In this case glucose uptake and lactate release were 2 times higher. Changes in glycogen level were observed three days after the last ethanol administration. The rats, survived after the abstinence period, revealed areas of perivascular myocardial necrosis. It is concluded that withdrawal syndrome plays an important role in pathogenesis of alcoholic cardiomyopathy.