Functional nitric oxide conjugate systems state/restored heart thiols of rats in modeling isadrine-pituitrin’s myocardial infarction using metabolite-tropic cardioprotector “Angiolin.

ABSTRACT

Background: According to modern researches, endothelial dysfunction (ED) is one of the primary pathogenetic elements of cardiovascular diseases (myocardial infarction [MI], ischemic heart diseases, cerebral ischemic stroke, atherosclerosis, arterial hypertension, pulmonary hypertension, heart failure, and dilated cardiomyopathy) as well as obesity, hyperlipidemia, diabetes and hyperhomocysteinemia. The aim of this work was to study the infl uence of potential metabolitotropic cardioprotector “Angiolin” on the parameters of conjugate systems nitric oxide (NO)/restored thiols in heart under isadrine-pituitrin MI. Methods: This study was performed on Wistar white rats weighing 190-210 g. Biochemical, immune-enzyme analysis and histoimmunechemical study were performed. Results: In histological sections of hearts of the rats receiving Angiolin in parenteral dosing 50 mg/kg 30 mins before each pituitrin injection the density of endothelial NOsynthase (NOS)-positive cells increased by 29% and the density of inducible NOSpositive cells decreased by 23.3%. In cytosolic fraction of myocardium homogenate NOS activity increased by 27%, the concentration of NO stable metabolites increased by 70% and the content of nitrosative stress marker nitrotyrosine decreased by 42% when compared with control group. At the same time in similar samples of heart homogenate the increase of restored thiol groups’ level by 53.3%, methionine - by 35.1%, cysteine - by 170% and activity of glutathione reductase - by 186% was noted. The administration of reference drug mildronate to the animals with MI in dose 100 mg/kg did not result in signifi cant changes of the studied parameters of thiol-disulfi de system and NO system of the heart when compared with control group. Conclusions: Angiolin does not infl uence directly on NOS in MI, but at the same time protects NO from nitrosative stress increasing restored equivalents of thioldisulfi de system.