[Antioxidant efficacy in the treatment of cardiac metabolism disorders during endotoxicosis].

Chronic experiments on dogs showed that antioxidant drugs (reamberin, ximedone, vitamin E) are highly effective in correcting the functional and metabolic disorders in myocardium under endogenous intoxication conditions. Recovery of the functional activity was accompanied by correction of the lipid metabolism of cardiac cell structures. One mechanism of the drug action is related to a decrease in the lipid peroxidation rate and phospholipase A2 activity in cardiac tissue structures.

[Studying efficacy of remaxol in the treatment of respiratory distress syndrome under endotoxicosis conditions].

Chronic model experiments on dogs showed that the development of respiratory distress syndrome under acute pancreatitis conditions is correlated with violation of metabolic processes in the lung tissue, which is caused by activation of the coagulation/lysis system and changes in the lipid metabolism. It is established that remaxol limits the development of inflammatory processes in lungs, produces correction of the lipid metabolism, and introduces positive changes in the coagulation system lung tissues under acute pancreatitis conditions.

[Correction of endogenous intoxication syndrome in acute pancreatitis].

The endogenous intoxication syndrome was determined with chronic experiments to correlate to functional and metabolic disturbances of liver and intestines under acute pancreatitis. The remaxol use therapy corrects endogenous intoxication syndrome that based on hepato- and enteroprotective medicine effects.

[Cardioprotective and lipid-regulating effects of etoxidol with respect to surgical endotoxinemia].

Chronic experiments on stray dogs with modeling peritonitis showed that a complex therapy involving etoxidol favors improvement of the electrophysiological and metabolic heart activity and provides correction of the lipid distress syndrome. It is established that the lipid regulating effect of etoxidol is related not only to a decrease in the intensity of lipid peroxidation (LPO), but also to the A2-phospholipasae activity of this drug.