Cardiac effects of bee venom in rats

To elucidate the possible effects of bee venom [BV] on cardiac electrophysiological properties in vivo, the inotropic and chronotropic properties of the isolated hearts in vitro, and the cardiac responsiveness to progressive adrenergic stimulation by isoproterenol. This randomized control study was conducted in the Physiology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt, from April to June 2010. This work was carried out on 22 female Wistar rats. Rats were allocated into 2 groups; BV-treated group [rats were treated with BV in a dose of 20 micro g/kg body weight, administered subcutaneously for 4 days], and the control group. Prior to sacrifice, the studied animals underwent electrocardiographic [ECG] assessments under anesthesia. Thereafter, isolated hearts were studied in a Langendorff preparation for their intrinsic properties, and their responses to beta-adrenergic stimulation. Following recovery, heart tissues were used for assessment of myocardial calcium content, and for histological examination. No abnormal ECG findings were observed in the BV-treated group. The BV treatment enhanced tension generation in the cardiac muscle in response to beta-adrenergic stimulation, and improved the inotropic cardiac reserve. Calcium content of the myocardial tissue of BV-treated group was significantly increased. Histological examination of the cardiac tissue of BV-treated group demonstrated preserved myofilament and mitochondrial ultrastructural integrity. The BV enhanced the cardiac inotropic reserve to beta-receptor agonists. Meanwhile, BV protected the heart against calcium overload-induced injury

Protective effects of vitamin E against myocardial ischemia/reperfusion injury in rats

To clarify the cardioprotective effects of a short course of vitamin E treatment [vit E] as compared with a nitric oxide donor, nitroglycerin [GTN] against ischemia-reperfusion induced heart injury in rats. This randomized control study was conducted in the Physiology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt from 1st June to 31 August 2009. This work was undertaken on 28 female Wistar rats weighing 150-200 gin. Rats were allocated into 4 groups; control group [non-treated], GTN-treated group [rats received GTN intraperitoneally 25 minutes before sacrifice, in a dose of 120 microg/kg body weight], vit E-treated group [rat received vit E by oral tubal feeding 16-20 hours before sacrifice, in a dose of 250 mg/rat], and vit E and GTN-treated group [rats received vit E and GTN as in both GTN-treated group and vit E-treated group]. After sacrifice, the hearts were excised and perfused in a Langendorff preparation and subjected to 30 minutes global ischemia and reperfused for 30 minutes, Following reperfusion, heart tissues were used for assessment of malondialdehyde [MDA] and nicotinamide adenine dinucleotide [NAD][+], and for histological examination. Vitamin E treatment resulted in an enhanced post-ischemic recovery of systolic function in vit E-treated groups [vit E-treated group, and vit E and GTN-treated group] compared to the control group. Post-ischemic recovery of coronary flow was enhanced in the vit E-treated group compared to the GTN-treated group. Post ischemic tissue degeneration indicators: MDA, and NAD[+] indicated a cardioprotective effect of vit E. Histological study revealed marked improvement of myocytes and mitochondrial structure in the vit E-treated group as compared with the control group. Preconditioning with vit E treatment afforded substantial recovery of post-ischemic contractile, and vascular functions compared to GTN treatment, the mechanism might involve less opening of mitochondrial permeability transition during postischemic reperfusion