NO-зависимый механизм кардиопротекторного действия фенибута при стрессорном нарушении сократительной функции сердца

A stressor action for 24 h reduces both ino- and chronotropic reserves of animal heart as evidenced by a decrease in rate growth increments of contraction and relaxation of the myocardium, left ventricular pressure (LVP), heart rate, and the maximum intensity of functioning (MIF) as compared to intact animals during testing for adrenoreactivity and maximum isometric load caused by clamping of the ascending part of the aortic arch. Blockade of NO-synthase leads to a high percentage of animal death during the stressor action, anesthesia, opening of the chest, and functional tests and causes marked reduction in the growth rates of contraction (+ dP / dt max) and relaxation (– dP / dt max) speed, LVP, heart rate, and MIF – on the average about 2 times ( p < 0.05) under load testing conditions as compared to a control group of stressed animals. Phenibut limits stress-induced violations of the myocardium contractility, as indicated by a higher growth of performance in stress tests – on the average about 1.8 times ( p < 0.05) in comparison to the control group of animals. The cardioprotective effect of phenibut is less pronounced when it is introduced on the background of the blockade of NO-ergic system. Under these conditions, there are cases of animal death, predominantly during the stressor action. The results obtained suggest that, for ensuring cardioprotective action of phenibut under conditions of stress-induced myocardial damage, it is necessary to provide for participation of nitric oxide system.