Cardioprotective effects of resveratrol following myocardial ischemia and reperfusion.

Resveratrol (RSV), a plant origin polyphenol, has shown beneficial cardiovascular effects. In this study, isolated hearts from male Wistar rats were studied using the Langendorff technique. Following 30 min stabilization, the hearts underwent 30 min global ischemia and 120 min reperfusion. The perfusion solution in the test group contained RSV (10 µM). Hemodynamics of the hearts, the markers of myocardial damage including creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and troponin I were studied during the study. Furthermore, the infarct size and the markers of oxidative stress including catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GPX) were assayed in the homogenates of the hearts. The release of nitrite from the hearts and the occurrence of ventricular arrhythmias were also monitored throughout the experiment. Resveratrol caused a significant improvement in the restoration of the mechanical performance of the hearts following myocardial ischemia and reperfusion (MIR). Besides, the infarct size, CK-MB, LDH, and troponin I declined in the test group. Besides, the cardiac release of nitrite increased, and the redox status of the heart was improved as indicated by the levels of CAT, SOD, GPX, and MDA. Finally, the treatment caused significant decreases in the occurrences of single and salvo arrhythmias, ventricular tachycardia, and ventricular fibrillation. The current study suggests strong cardioprotective and antiarrhythmic effects for RSV following MIR.

Nitric oxide plays a pivotal role in cardioprotection induced by pomegranate juice against myocardial ischemia and reperfusion.

Pomegranate juice (Pg) has demonstrated cardiovascular beneficial effects. The current research intends to investigate the roles of nitric oxide (NO) and antioxidants in Pg-induced cardioprotection against ischemia and reperfusion (I/R). Isolated hearts from anesthetized rats were subjected to 30-min global ischemia followed by 120-min reperfusion. The hearts in the test groups were treated with Pg, NG -nitro-L-arginine methyl ester (L-NAME) or both throughout the experiment. In Pg group, left ventricular developed pressure, rate of rise in left ventricular pressure (dp/dt max), and rate pressure product were 83%, 55%, and 127%, respectively, higher than those of the control group (p < 0.05). The infarct size declined to less than 40% (p < 0.0001), and biomarkers of myocardial damage including creatine kinase-MB, lactate dehydrogenase, and troponin-I, showed significant reductions (59%, 36%, and 94%, respectively) compared with the control. Furthermore, the indices of oxidative status including superoxide dismutase, glutathione peroxidase, catalase, and malondialdehyde showed significant improvement (2.4, 1.7, 1.9, and 2.4 fold, respectively). Most of these effects were mainly blocked by L-NAME. These results suggest potent cardioprotective effects for Pg against myocardial I/R injury. The current results suggest a key role for NO for this cardioprotection; however, other mechanisms seem to be also involved.