Abstract:
Adrenaline damage to the myocardium is an important element in the pathogenesis ofmyocardial infarction in humans. Despite the use of modern methods of treatment of myocardial infarction, the issue of cardioprotection of reperfusion myocardial damage remains open. Promising in this direction is the use of quinazolone derivatives, which have already shown cardioprotective properties in other models of myocardial infarction.The aim of the study was to establish morphological changes in the conditions ofadrenaline myocardiodystrophy (AMD) against the background of the introduction ofthe compound PC-66 and amiodarone in rats. The study was performed on 100 nonlinearrats of both sexes weighing 165-220 g, divided into four groups of 25 animals each:1 - intact rats; 2 - rats with a model of adrenaline myocardial infarction without treatment(control); 3 - rats with AMD treated with amiodarone (10 mg/kg, intraperitoneally);4 - rats with AMD treated with compound PC-66 (10 mg/kg, intraperitoneally). It wasfound that control rats under conditions of cardiotoxic dose of adrenaline in the leftventricular myocardium for up to 8 days of the experiment does not fully restore themyocardial structure, dystrophic and necrobiotic changes were found in bothcardiomyocytes and walls of vessels of a blood microcirculatory channel of amyocardium. Course intraperitoneal administration to rats of the compound PC-66 inthe conditions of adrenaline myocardial infarction as well as amiodarone, contributesto the attenuation of signs of dystrophic and destructive processes. The degree ofprotective effect on the myocardium under conditions of cardiotoxic dose of adrenalinecompound PC-66 was not lower to the reference drug - amiodarone. Thus, it ismorphologically confirmed that in adrenaline myocardial infarction the compoundPC-66, similar to the action of amiodarone, has a cardioprotective effect.
