Cardioprotective effects of resveratrol following myocardial ischemia and reperfusion
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ORIGINAL ARTICLE
Cardioprotective effects of resveratrol following myocardial ischemia and reperfusion Hamideh Kazemirad1 · Hamid Reza Kazerani1 Received: 28 March 2020 / Accepted: 8 July 2020 © Springer Nature B.V. 2020
Abstract 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. Keywords Resveratrol · Isolated heart · Ischemia and reperfusion · Oxidative stress · Arrhythmia
Introduction Cardiac arrhythmias following myocardial ischemia and reperfusion (MIR) are the leading cause of mortality in patients with ischemic heart disease. MIR lead to a cascade of events, which eventually leads to cardiac damage and the occurrence of arrhythmias. Several intracellular and electrophysiological disturbances such as accumulation of intracellular Na+, Ca2+, and H+ ions, the opening of mitochondrial permeability transition pore (mPTP), excessive generation of reactive oxygen substances (ROS), apoptosis, and autophagy are involved in the pathogenesis of MIR-induced injury [1]. Intracellular calcium overload results in hyperactivity of the sarcolemmal sodium-calcium exchanger. Since three sodium ions are exchanged with one calcium ion, the transporter * Hamid Reza Kazerani [email protected]; [email protected] 1
Department of Physiology, The School of Veterinary Medicine, Ferdowsi University of Mashhad, PO Box: 91775‑1793, Mashhad, Iran
protein is electrogenic. This leads to the hypopolarization of cardiomyocytes early after repolarization, a phenomenon called delayed afterdepolarization. In case this signal is strong enough to reach the threshold, ectop
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