Cardiovascular risk factors in L-NAM E hypertension

In a previous study, hypertension was induced by administration of L-NAME for 1, 2 and 4 weeks. Hypertension was prevented when L-NAME was combined with L-arginine but not with dipyridamole. To study the changes in ECG, cardiac weights and plasma lipids associated with L-NAME hypertension. Wistar rats were allocated into a control group, 3 groups of rats that received L-NAME [20 mg/kg] for 1, 2 and 4 weeks, and 2 other groups that received L-NAME in the same dose for 2 weeks combined with L-arginine [40mg/kg] or dipyridamole [3mg/ kg]. The absolute weight of left ventricle [LV] and whole heart [WH] were significantly increased in L-NAME 4 weeks group, but such significant increase was lost when corrected for body weight [LV/BW and WH/BW]. In L-NAME and L-arginine 2 weeks group, there was no change in absolute or relative weights, whereas in the L-NAME and dipyridamole 2 weeks group, there was significant decrease in LV, WH and LV/BW. Concerning ECG parameters, there was no significant difference amongst control group and L-NAME I, 2 and 4 weeks groups as regards P-R interval, QRS complex and R-wave voltage. Both Q-To and Q-Tc intervals were significantly shortened in L-NAME 4 weeks group than control, L-NAME I week and 2 weeks groups. In L-NAME and L-arginine 2 weeks group, P-R interval was significantly shorter than control group. Also, L-NAME and dipyridamole 2 weeks group showed significant in R wave voltage than control and L-NAME 2 weeks groups. Treatment for 2 weeks with L-arginine or dipyridamole shortened Q-To and Q-Tc than control or L-NAME 2 weeks groups. In NAME-treated rats for I, 2 and 4 weeks, there was no significant changes in plasma levels of total cholesterol, HDL-cholesterol and LDL- cholesterol, nor atherogenic index or triglycerides. L-NAME hypertension up to 4 weeks duration was not associated with cardiac hypertrophy or ECG changes. Also, the lipid profile was not significantly modified from the normal pattern

Hematological and cardiac effects of excess zinc in rats

In this work administration of zinc sulphate at a dose of 20 mg/kg/day. 6 days/week for 4 successive weeks, resulted in significant decrease in RBCs count, hemoglobin content, hematocrit value and mean corpuscular hemoglobin concentration in zinc treated group compared to control group. Biochemical studies showed significant decrease in plasma triglyceride, and malondialdehyde levels in zinc treated group compared to control group. However, non significant difference was found between the two groups as regards plasma zinc level. ECG study demonstrated significant increase in heart rate [HR] in zinc treated group compared to control group. This was accompanied by shortening of QRS and prolongation in Q-Tc durations in zinc treated group compared to control group. In vitro study of isolated hearts perfused in a Langendorff preparation, significant increase in basal HR was shown in zinc treated group compared to control group. The maximal HR upon isoproterenol infusion [ISU], when expressed as percentage ratio from baseline values, showed significant decrease in zinc treated group compared to control group. As regards baseline peak tension [PT] and peak tension/left ventricular weight [PT/LV,], significant increase was found in zinc treated group compared to control group. Also, the PT maximal response upon ISU infusion, either absolute or upon correction of left ventricular weight, showed significant increase in zinc treated group. Significant shortening in baseline time to peak tension [TPT] and half relaxation time [l/2RT,] were noticed in zinc treated group compared to control group. However, basal myocardial flow rate [MFR] as well as MFR/L V showed non significant difference between the 2 studied groups. Post ischemic reperfusion responses showed non significant difference as regards HR between the 2 studied groups. The recovery of PT and PT/LV were significantly higher at 20, 25, and 30 minutes of reperfusion in zinc treated group compared to control group. As regard TPT reperfusion values, significant prolongation at 10 minute was noticed in zinc treated group compared to control group. However 1/2RT, MFR and MFR/LV reperfusion values, non significant differences were recorded between the two studied groups. From this study, it can be concluded that zinc administration at a dose of 20 mg/kg/day for 4 successive weeks, has a protective effect against the risk of atherosclerosis and oxidative stress in vivo. Also, zinc treatment maintained or even enhanced the intrinsic cardiac functions, both chronotropic and inotropic, and their responses to B-adrenergic stimulation. In addition, zinc proved to be a beneficial cardioprotective agent as it attenuated the detrimental effects of post-ischemia reperfusion on the myocardial contractility

Effects of hemorrhage on myocardial metabolism

In vivo and in vitro studies were done to study the effects of severe haemorrhage [30%] of blood volume on cardiac metabolism. Induction of bleeding resulted in a significant increase in glucose uptake at 60 minutes post haemorrhage. Insignificant changes in pyruvate production and in glycerol release were observed Pre-treatments of rats with propranolol did not significantly affect the response of the heart to haemorrhage Also pretreatment with aprotinin resulted in only a significant release of glycerol by the heart In vitro results on the effects of shock plasma on the normal heart revealed an insignificant increase in glucose uptake and a significant glycerol release. The mechanisms underlying these effects are discussed

protective effect of vitamin E in stress-induced myocardial lesion in rats

The effect of vitamin E on the changes induced in the rat heart by chronic isoproterenol treatment was examined. Administration of isoproterenol [1 mg/kg] daily for 7 consecutive days has evoked significant hypertrophy in all cardiac chambers. The basal heart rate in chronically isoproterenol-treated rats was lower than in saline-treated control rats [315 +/- 9 vs 348 +/- 16 b.p.m. P < 0.05]. Also the chronotropic responses to isoproterenol graded infusion in sequential doses were significantly higher in control rats than in chronically isoproterenol-treated rats [145 +/- 23 vs 92 +/- 13 maximal increments in heart rate b.p.m., P < 0.05]. Pretreatment with vitamin E has only prevented hypertrophy in atria but did not modify the hypertrophic response in ventricles of isoproterenol-treated rats. Moreover, it ameliorated the difference in heart rate between the isoproterenol-treated and the saline-treated rats both in basal condition [306 +/- 10 vs 330 +/- 12, n.s.] and in response to graded stimulation by isoproterenol infusion [115 +/- 19 vs 117 +/- 14 maximal increments in heart rate b.p.m., n.s.]. The protective effect of antioxidant vitamin E against the reduction in chronotropy and chronotropic responses in chronically isoproterenol-treated rats, may point to the role of oxygen free radicals in mediation of these functional cardiac disturbances

effect of vitamin E and inderal on cardiac lesions induced by adrenergic-mediated stresses

The protective effect of vitamin E [300 mg/kg, daily] and inderal [1 mg/kg, daily] on the cardiac lesions induced in rats by two types of stress was evaluated. Rats were exposed to repeated stress by restraint or water immersion [2 hr daily for 4 consecutive days]. In both types of stressed rats, significant hypertrophy was developed in atria, right ventricle, left ventricle, and whole heart. While pretreatment with vitamin E has prevented hypertrophy in all chambers in both stresses, inderal pretreatment was only effective in prevention of atrial hypertrophy. In rats chronically stressed 'by water immersion the heart rate was significantly lower than in the non-stressed control rats both in the basal condition [293 +/- 26 vs 348 +/- 16 b.p.m., p < 0.001] and in the maximal increments in response to graded isoproterenol infusion [30 +/- 17 vs 145 +/- 23, P. < 0.01]. Vitamin E pretreatment has ameliorated the difference between the group subjected to chronic water immersion and control group in basal heart rate but not in the chronotropic responses to isoproterenol stimulation, whereas pretreatment with inderal was ineffective in modifying both. Chronic restraint, on the other hand, did not lead to significant reduction in heart rate or chronotropic responses to isoproterenol stimulation. The protective effect of vitamin E against both hypertrophy and heart rate changes in rats subjected to such adrenergic-mediated stresses may provide important evidences for the role of free radicals and lipid peroxidation in the pathogenesis of cardiac lesions induced by endogenous catecholamines