Contractile function of the heart and the state of some stages of lipid metabolism during acute diphtheritic intoxication

Acute diphtheritic intoxication was modeled in rabbits by intravenous administration of native diphtherin (0.3 minimal lethal dose per 1 kg body weight). The contractile function of the left and right ventricles (peak systolic pressure under conditions of basal hemodynamics and during 5-sec occlusion of the aorta and pulmonary artery, respectively) was estimated 1, 3 and 5 days after the start of the pathological process, the intensity of lipid peroxidation was evaluated by measuring the content of TBA- reactive products in the myocardium. Impairment of the contractile function of both ventricles was observed in the course of intoxication. The level of TBA-reactive products in the left ventricle signifi cantly decreased on day 1, but then returned to normal. Thus, impairment of the contractile function of the left ventricle at the early stages of diphtheritic intoxication is not mediated by activation of lipid peroxidation in cardiomyocytes. © 2009 Springer Science+Business Media, Inc

Activities of some caspase cascade enzymes and myocardial contractility in experimental left ventricular focal ischemia

Focal left ventricular ischemia was modeled in male Chinchilla rabbits. Activities of caspase-3 and caspase-8 in the left and right ventricular myocardium and myocardial contractility were studied after 1, 3, and 5 days. Caspase-3 activity increased significantly in the left ventricular peri-infarction zone and right ventricular myocardium, while caspase-8 activity did not differ from the control. Left ventricular contractility decreased significantly and the hemodynamic load of the right ventricle sharply increased. These results attest to induction of the internal (mitochondrial) pathway of apoptosis in myocardial cells most likely caused by left ventricular hypoxia and right ventricular overload. © 2011 Springer Science+Business Media, Inc

Contractile function of the heart and the state of some stages of lipid metabolism during acute diphtheritic intoxication

Acute diphtheritic intoxication was modeled in rabbits by intravenous administration of native diphtherin (0.3 minimal lethal dose per 1 kg body weight). The contractile function of the left and right ventricles (peak systolic pressure under conditions of basal hemodynamics and during 5-sec occlusion of the aorta and pulmonary artery, respectively) was estimated 1, 3 and 5 days after the start of the pathological process, the intensity of lipid peroxidation was evaluated by measuring the content of TBA- reactive products in the myocardium. Impairment of the contractile function of both ventricles was observed in the course of intoxication. The level of TBA-reactive products in the left ventricle signifi cantly decreased on day 1, but then returned to normal. Thus, impairment of the contractile function of the left ventricle at the early stages of diphtheritic intoxication is not mediated by activation of lipid peroxidation in cardiomyocytes. © 2009 Springer Science+Business Media, Inc

Activities of some caspase cascade enzymes and myocardial contractility in experimental left ventricular focal ischemia

Focal left ventricular ischemia was modeled in male Chinchilla rabbits. Activities of caspase-3 and caspase-8 in the left and right ventricular myocardium and myocardial contractility were studied after 1, 3, and 5 days. Caspase-3 activity increased significantly in the left ventricular peri-infarction zone and right ventricular myocardium, while caspase-8 activity did not differ from the control. Left ventricular contractility decreased significantly and the hemodynamic load of the right ventricle sharply increased. These results attest to induction of the internal (mitochondrial) pathway of apoptosis in myocardial cells most likely caused by left ventricular hypoxia and right ventricular overload. © 2011 Springer Science+Business Media, Inc

Assessment of caspase-3 activity in rabbit myocardial tissue during experimental hemodynamic overload of the left ventricle of the heart

It's well known that chronic overload of the cardiac left ventricle is accompanied by an increase in the cardiomyocyte apoptosis rate. However direction and extent of programmed cell death changes under an acute overload of the left ventricle still requires detailed investigation. Caspase-3 activity has been investigated in myocardium of rabbits on the 1,3 and 5 days after modeling of left ventricle hemodynamic overload caused by surgical narrrowing of the ascending aorta. Control group included intact animals. It was found that caspase-3 activity significantly increased in both ventricles on day 1; it increased more than twofold above controls on day 3; it began to decrease by day 5. On the basis of the obtained data it was concluded that: an acute hemodynamic overload of the left ventricle is a cause of apoptosis acceleration in the myocardial tissue of both cardiac ventricles during first days of the investigated process

Assessment of caspase 3 activity in rabbit myocardial tissue during experimental hemodynamic overload of the left ventricle of the heart

It is well known that chronic overload of the cardiac left ventricle is accompanied by an increase in the cardiomyocyte apoptosis rate. However, direction and extent of changes in programmed cell death under an acute overload of the left ventricle still requires detailed investigation (as its pathogenesis significantly differs from chronic overload). Caspase-3 activity has been investigated in left ventricle myocardium of rabbits on days 1, 3, and 5 after modeling of left ventricle hemodynamic overload caused by experimental stenosis of the ascending aorta. Control group included intact animals. It was found that caspase-3 activity significantly increased in both ventricles on day 1; it increased more than twofold above control values on day 3 and decreased up to nearly control values on day 5. Based on these data it was concluded that the acute hemodynamic overload of the left ventricle may be a cause of increased apoptosis in the myocardial tissue of both cardiac ventricles during first days of the pathological process. © Pleiades Publishing, Ltd., 2011

Assessment of caspase 3 activity in rabbit myocardial tissue during experimental hemodynamic overload of the left ventricle of the heart

It is well known that chronic overload of the cardiac left ventricle is accompanied by an increase in the cardiomyocyte apoptosis rate. However, direction and extent of changes in programmed cell death under an acute overload of the left ventricle still requires detailed investigation (as its pathogenesis significantly differs from chronic overload). Caspase-3 activity has been investigated in left ventricle myocardium of rabbits on days 1, 3, and 5 after modeling of left ventricle hemodynamic overload caused by experimental stenosis of the ascending aorta. Control group included intact animals. It was found that caspase-3 activity significantly increased in both ventricles on day 1; it increased more than twofold above control values on day 3 and decreased up to nearly control values on day 5. Based on these data it was concluded that the acute hemodynamic overload of the left ventricle may be a cause of increased apoptosis in the myocardial tissue of both cardiac ventricles during first days of the pathological process. © Pleiades Publishing, Ltd., 2011

Assessment of caspase-3 activity in rabbit myocardial tissue during experimental hemodynamic overload of the left ventricle of the heart

It's well known that chronic overload of the cardiac left ventricle is accompanied by an increase in the cardiomyocyte apoptosis rate. However direction and extent of programmed cell death changes under an acute overload of the left ventricle still requires detailed investigation. Caspase-3 activity has been investigated in myocardium of rabbits on the 1,3 and 5 days after modeling of left ventricle hemodynamic overload caused by surgical narrrowing of the ascending aorta. Control group included intact animals. It was found that caspase-3 activity significantly increased in both ventricles on day 1; it increased more than twofold above controls on day 3; it began to decrease by day 5. On the basis of the obtained data it was concluded that: an acute hemodynamic overload of the left ventricle is a cause of apoptosis acceleration in the myocardial tissue of both cardiac ventricles during first days of the investigated process