[COMPARATIVE STUDY OF THE HEART FUNCTIONAL RESERVE UNDER STRESS-INDUCED BLOCKADE OF NO-ERGIC SYSTEM AND GABA-A RECEPTORS IN RATS.].

Cardiac contractility in rats was decreased after 24-h immobilization-painful stressing, as indicated by lower growth rate of myocardium contraction and relaxation, LVP, heart rate, and maximum functioning intensity (MIF) in comparison to intact group during functional tests on adrenoreactivity and maximum isometric workload. Stressed animals pretreated with the GABA-A receptors blocker bicuculline (2 mg/kg, i.p.

[Cardioprotective effect of the new derivative of glutamic acid - glufimet in acute immobilization-painful stress in animals of different ages].

The effect of the 24-hour immobilization-painful stress on myocardial contractility of young (6-month), middle-aged (12-month) and old (24-month) female rats was studied. It was identified a reduction of the functional reserve of the heart, which showed a smaller growth rates of contraction and relaxation of the myocardium (+ dP/dt max and -dP/dt max), left ventricular pressure (LVP) and the maximum intensity of the functioning of the structures (MIFS) under increased pre- afterload and adrenergic stimulation of the heart, especially pronounced in the group of 24-month old rats. The animals of all ages treated before and after stressing glufimet in a dose 29 mg/kg, have higher rates of growth + dP/dt max, -dP/dt max, LVP and MIFS during load tests, most significant rates of growth are noticed in older rats compared with the young and middle-aged.

Effects of a New Glutamic Acid Derivative on Myocardial Contractility of Stressed Animals under Conditions of Nitric Oxide Synthesis Blockade.

Glufimet (glutamic acid derivative) in a dose of 28.7 mg/kg limited the reduction of the cardiac functional reserve in animals subjected to 24-h stress under conditions of nonselective NO synthase blockade with L-NAME (10 mg/kg). Adrenoreactivity and increased afterload tests showed that the increment of myocardial contraction/relaxation rates, left-ventricular pressure, and HR were significantly higher in glufimet-treated stressed animals with NO synthesis blockade than in animals which received no glufimet.

[NO-DEPENDENT MECHANISM OF THE CARDIOPROTECTIVE ACTION OF PHENIBUT ON STRESS-INDUCED VIOLATION OF CONTRACTILE FUNCTION OF THE HEART].

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.

[Cardioprotective properties of new glutamic acid derivative under stress conditions].

The effect of new glutamic acid derivative on the cardiac ino- and chronotropic functions has been studied in experiments on rats exposed to 24-hour immobilization-and-pain stress. It is established that glutamic acid derivative RGPU-238 (glufimet) at a dose of 28.7 mg/kg increases the increment of myocardial contractility and relaxation rates and left ventricular pressure in stress-tested animals by 13 1,1, 72.