Search

In model experiments reproducing the holiday heart syndrome in rats, a discrepancy between the depolarization of the right and left atria has been revealed, which manifested by an atypical arrangement of positive and negative cardiopotentials in the cardioelectric field on the body surface during the P wave and the absence of inversion of the areas of cardioelectric potentials before the onset of P waves in lead II ECG from the limbs. [ABSTRACT FROM AUTHOR]

A translational rat model of chronic heart failure was employed to examine the cardioprotective effect of fabomotizole hydrochloride. Fabomotizole therapy for 28 days (15 mg/kg/day intraperitoneally) restored inotropic function of the left ventricle and increased ejection fraction from 54±3 to 65±3% (p=0.001). The inotropic function returned to normal against the background of significantly reduced myocardial expression of angiotensin (p=0.01) and glucocorticoid (p=0.03) receptors and significant increased expression of sigma-1 receptors (p=0.04). Inhibition of abnormal expression of angiotensin and glucocorticoid receptors responsible for activation of the pathological cascades underlying the postinfarction remodeling of the left ventricle as well as activation of the expression of cytoprotective sigma-1 receptors are viewed as the key features of the cardioprotective action of fabomotizole hydrochloride. [ABSTRACT FROM AUTHOR]

Series of benzylidene and benzyl derivatives of 1,2,5-trimethyl-, 2,2,6,6-tetramethylpiperidyl-, and tropylamines were synthesized and screened for anti-ischemic activity in rats. The lead compound was identified as 2,2,6,6-tetramethyl-N-(3,4,5-trimethoxybenzyl)piperidin-4-amine, the anti-ischemic activity of which was statistically significantly greater than that of the reference drug trimetazidine in a myocardial subendocardial ischemia model. [ABSTRACT FROM AUTHOR]