Role of A2-adrenoceptors in Rat Heart with the Model of Myocardial Infarction

Chronic adrenergic and angiotensin-energic stimulation of the heart muscle is one of the main causes of the onset and development of heart failure. α2 -AR is widespread in the cardiovascular system and can be further applied and introduced into the heart s regenerative cell therapy. This study s objective was to study the effect of α2 -AR stimulation on the performance of an isolated heart in rats with a model of myocardial infarction. To study the mechanisms of MI, experiments were carried out according to the classical technique of H. Selye - ligation of the anterior branch of the left coronary artery and perfusion of a Langendorff heart with a model of myocardial infarction. We studied the parameters of myocardial activity by changes in heart rate, as well as the left ventricle pressure (LVP), and the CF (dp/dtmax)/(dp/dtmin) of the left ventricle. Coronary dilator activity was assessed by measuring the outflow of the perfusion solution through the coronary arteries. The amplitude of the left ventricle s pressure wave after application of the α2 -AR agonist clonidine hydrochloride at a concentration of 10-6 M to the perfused solution increased by 44% (p≤0.05) from the initial values. The rate of contraction and the rate of relaxation of the left ventricular myocardium also increased by 20% (p≤0.05) and 37% (p≤0.05), respectively. The activation of α2-AR in adult rats isolated hearts with a model of myocardial infarction caused a decrease in heart rate by 18% (p≤0.05) and CF by 2% (p≤0.05).