Differential effects of vitamin E supplementation on cardiovascular risk factors and on cardiac vulnerability to ischemia and reperfusion in rats

ABSTRACT

The present study was performed to examine the effects of vitamin E on hemodynamics, electrocardiogram [ECG] pattern, plasma levels of lipid profile, enzymes reflecting myocardial cell integrity creatine kinase [CK] and lactate dehydrogenase [LDH] and rate of lipid peroxidation as well as on myocardial performance after ischemia-reperfusion injury in isolated rat hearts. Vitamin E-treated rats were injected with vitamin E in a dose of 4 mg/100g body weight [b.w.] daily, for 6 consecutive days. Control rats were treated with vitamin E-solvent, daily, for the same duration. Then, rats were sacrificed, and the isolated heart were subjected to 30 min. ischemia followed by 30 min period of reperfusion. The present study demonstrated that administration of vitamin E in normal rats did not produce any appreciable hemodynamic effects as regards heart rate [HR], mean arterial pressure [MAP,], and pressure rate product[PRP]. The ECG pattern showed no arrhythmias or ischemic changes compared to control group. Concerning changes in plasma lipid profile, vitamin E-treated rats showed significant reduction in both total cholesterol [TC], and low density lipoprotein-cholesterol [LDL-C] Moreover, high density lipoprotein-cholesterol / total cholesterol [HDL-C/TC] was significantly elevated, in contrast to a non significant decrease in both low density lipoprotein-cholesterol/ total cholesterol [LDL-C /TC] and LDL-C /HDL-C ratios, when compared with controls. Myocardial cellular integrity, estimated by the plasma level of CK and LDH, was preserved by the administration of vitamin E, revealed evidently by the significant decrease in CK and LDH release in plasma of rats treated with vitamin E as compared to control rats. Moreover, the plasma level of malondialdehyde, as an index for the degree of lipid peroxidation, was significantly reduced. The preischemic, baseline activity of the isolated hearts obtained from rats treated with vitamin E, revealed non significant changes in myocardial inotropy except for prolongation of half relaxation time. Also there was a significant reduction in both heart rate and LDH release in the coronary effluent, while there was a non significant change in tile coronary flow rate. The results of the isolated hearts subjected to reperfusion following 30 minutes ischemic period, showed that vitamin E decreased the detrimental effect of reperfusion on the inotropic activity observed in the control group, evident by superior recovery of postischemic reperfusion myocardial functions. Manifested by elevated peak developed tension, and tension generation per unit time, concomitant with shortening of time to peak tension, and half relaxation time, along the reperfusion period. In addition, the percentage recovery of the heart rate was better during the whole reperfusion period but the difference was statistically significant only at 15-minute of reperfusion, and as well myocardial flow rate percentage .showed significant superior recovery in vitamin E-treated rat hearts. Moreover, there was a significant reduction in both CK and LDH release in the coronary effluent of vitamin E treated rat hearts, compared to control hearts. It could be concluded that vitamin E administration has a favorable potential against the risk of atherosclerosis and lipid peroxidation and as well it may attenuate the detrimental effects of postischemic reperfusion on the myocardial contractility