Yuriyiv K. Oxidative and cholinergic factors in the mechanisms of necrotic process development in the myocardium of animals of different sex.

The dissertation is delicated to the examination of the role of oxidative stress, disturbance of cholinergic regulation and sexual features in the mechanisms of myocardium damaged by adrenaline. It was established that in condition of myocardium damaged by adrenaline arise disorder of dynamic equilibrium between activity of free-radical processes and system of antioxidant defence with the accumulation of primary and secondary products of lipoperoxidation especially in males, nitrogen oxide system with more considerable decrease of it maintenance in the tissue of atriums of males’ hearts. Disturbance of nervous-mediator processes in myocardium atriums and ventricles depends on sex of animals. Activation of the nitrogen oxide system (by L-arginine, 600 mg/kg) in myocardium in condition of its damage, decreases the percent of necrotic cardiomyocytes, products of lipoperoxidation, increases activity of enzymatic and non enzymatic links of antioxidant defence, normalizates sensitivity of cholinergic receptors, increases content of acetylcholine and reduces it enzymatic hydrolysis, especially in females’ atriums. Inhibition of the nitrogen oxide system activity (by L-NAME, 25 mg/kg) in the conditions of myocardium damage, increases the percent of necrotic cardiomyocytes, especially in males, reduces activity of nitrogen oxide system, promotes more considerable accumulation of lipoperoxidation products in myocardium of ventricles. In despite of antioxidants system activation (superoxidedismutase and katalase), inhibition of the nitrogen oxide system activity promotes decreases of nitrite anion and urea maintenance (mainly in myocardium of ventricles), causes development of disfunction of the nervous regulation in males (predominance of adrenergic regulation), in females (cholinergic regulation), decreases sensitivity of the cholinergic receptors in females, decreases of the acetylcholine maintenance and decreases of cholinesterase activity, especially in the atriums.