Vitamin E attenuates myocardial ischemia-reperfusion injury in murine AIDS

被引：6

作者：

Chen Y. ^{[1
,2
]}

Davis-Gorman G. ^{[2
]}

Watson R.R. ^{[1
,3
]}

McDonagh P.F. ^{[2
]}

机构：

[1] Div. of Health Prevention Science, College of Public Health, University of Arizona, Tucson

[2] Coll. of Cardiovasc./Thorac. Surgery, School of Medicine, University of Arizona, Tucson

[3] Div. of Health Prevention Science, College of Public Health, University of Arizona, Tucson, AZ 85724

来源：

Cardiovascular Toxicology | 2002年 / 2卷 / 2期

基金：

美国国家卫生研究院;

关键词：

Ischemia-reperfusion injury; Murine AIDS; Vitamin E;

D O I：

10.1385/CT:2:2:119

中图分类号：

学科分类号：

摘要：

The incidence of myocardial infarction in patients who have the aquired immunodeficiency syndrome (AIDS) is increasing. However, no effective therapeutic agents have been discovered to reduce myocardial ischemia-reperfusion (I/R) injury in pathologies associated with AIDS. The aim of this study was to determine if infarct size is increased in murine AIDS after I/R injury and if I/R injury could be attenuated with vitamin E supplementation. Three groups of mice were studied: control, murine AIDS, and murine AIDS with vitamin E supplementation. Anesthetized mice were subjected to 30 min of left anterior descending coronary artery occlusion and 120 min of reperfusion. The hearts in mice that had murine AIDS had a larger infarct size compared to controls after I/R injury. Vitamin E supplementation significantly reduced infarct size and inhibited polymorphonuclear neutrophil (PMN) CD11b expression (p < 0.05). However, vitamin E supplementation did not affect PMN reactive oxygen species (ROS) production and platelet CD62p expression. These results suggest that the reduction of myocardial I/R injury with vitamin E supplementation may be the result of the inhibition of PMN CD11b expression. Vitamin E may be a promising prophylactic agent for the reduction of the severity of myocardial I/R injury in patients who have AIDS.

引用

页码：119 / 127

页数：8

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