Sethi R, Takeda N, Nagano M, Dhalla N S
Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, Manitoba, Canada.
J Cardiovasc Pharmacol Ther. 2000 Jan;5(1):51-8. doi: 10.1177/107424840000500107.
Vitamin E (Vit E), an antioxidant, is considered to prolong survival in patients and animals after myocardial infarction. Because myocardial infarction is associated with arrhythmia and heart dysfunction, this study tested the hypothesis that early treatment with Vit E reduces mortality because of its protective effects against arrhythmia and cardiac dysfunction induced by acute myocardial infarction.
Rats were randomly divided into 4 groups: sham control, myocardial infarcted, Vit E-treated sham control, and Vit E-treated infarcted animals. Myocardial infarction was induced by ligation of the left anterior descending coronary artery. Treated animals received Vit E (25 mg/kg/d) through a gastric tube beginning 1 hour after the coronary occlusion, whereas control rats received tap water.
Electrocardiograms (lead II) at 1, 3, 7, and 21 days after coronary occlusion in the untreated animals showed ST-segment elevation, abnormal Q waves, premature ventricular complex (PVC), and QTc prolongation. Conversely, Vit E-treated rats showed attenuated ST-segment changes, fewer abnormal Q waves, and decreased incidence of PVC after coronary occlusion. Total mortality was reduced from 38% to 16%, whereas the infarct size was decreased from 44.2% to 22.3% in infarcted rats treated with Vit E. The depression in left ventricular function as well as elevation of malondialdehyde content and conjugated diene formation in the 21-day infarcted rat hearts were prevented by Vit E treatment.
These results indicate that Vit E may exert beneficial effects on the heart by reducing oxidative stress in acute myocardial infarction.
维生素E(Vit E)作为一种抗氧化剂,被认为可延长心肌梗死后患者及动物的生存期。由于心肌梗死与心律失常和心脏功能障碍相关,本研究检验了以下假设:早期使用Vit E治疗可降低死亡率,因为其对急性心肌梗死所致的心律失常和心脏功能障碍具有保护作用。
将大鼠随机分为4组:假手术对照组、心肌梗死组、Vit E治疗的假手术对照组和Vit E治疗的梗死动物组。通过结扎左冠状动脉前降支诱导心肌梗死。治疗组动物在冠状动脉闭塞后1小时开始通过胃管给予Vit E(25 mg/kg/d),而对照组大鼠给予自来水。
未治疗动物在冠状动脉闭塞后1、3、7和21天的心电图(II导联)显示ST段抬高、异常Q波、室性早搏(PVC)和QTc延长。相反,Vit E治疗的大鼠在冠状动脉闭塞后ST段变化减轻、异常Q波减少且PVC发生率降低。在接受Vit E治疗的梗死大鼠中,总死亡率从38%降至16%,梗死面积从44.2%降至22.3%。Vit E治疗可预防21天梗死大鼠心脏的左心室功能降低以及丙二醛含量升高和共轭二烯形成增加。
这些结果表明,Vit E可能通过减轻急性心肌梗死中的氧化应激对心脏发挥有益作用。