Cardioprotective effect of energostim during occlusion of coronary artery.

Experiments on dogs showed that energostim, a directly acting antihypoxant, injected 15 min after occlusion of the upper one-third of the left descending branch of the interventricular coronary artery produced a pronounced cardioprotective effect. The effect was confirmed by electron microscopy (evaluation the necrotic focus), biochemical tests of the heart and blood, and changes in intracardiac hemodynamics (recovery of systolic and diastolic functions). The cardioprotective effect of energostim greatly surpasses that of routine therapy applied during acute myocardium infarction.

Subcellular and molecular mechanisms of the effects of cardiac glycosides and angiotensin-converting enzyme inhibitors on contractile function and energy conversion in myocardial myofibrils under normal conditions and during acute cardiac insufficiency.

Experiments on skinned and hybrid myocardial fibers isolated from normal dogs and animals subjected to 120-min occlusion of the anterior interventricular branch of the coronary artery showed that in contrast to cardiac glycosides, angiotensin-converting enzyme inhibitors suppress contractile ability of myocardial myofibrils in a dose-independent manner within the concentration range of 10(-12)-10(-4)M. This effect is accompanied by a decrease in fiber relaxation rate most pronounced in the presence of captopril. Actin, the major protein of fine filaments is the target for b-acetyldigoxin, K-strophanthin, captopril, enalapril, and trandolapril in myocardial myofibrils.