The effects of murine AIDS and ethanol consumption on the severity of myocardial ischemic injury

Cardiovascular complications are prevalent in patients with AIDS. Cardiovascular complications, particularly ischemia-reperfusion injury, may be severe in AIDS patients. The pathology underlying cardiovascular complications in AIDS patients is unclear. Perhaps interplay of several pathologic factors amplifies the response to ischemia. Murine retrovirus (LP-BM5) induced murine AIDS is the best model of human AIDS research because LP-BM5 causes similar immune changes. Ethanol consumption has the advantage and disadvantage to health. The aim of this study was to determine if chronic ethanol consumption influences pathological changes caused by murine AIDS, specifically in cardiovascular complications, and if vitamin E supplementation could attenuate cardiovascular injury by murine AIDS. In our present study, we found that retrovirus infection enhanced neutrophil CD11b expression and ROS production, increased platelet CD62p and platelet microparticle formation, exaggerated coronary permeability to macromolecules and caused a severe myocardial ischemia-reperfusion injury. Chronic ethanol consumption down-regulated neutrophil CD11b expression, but neutrophil ROS production, platelet CD62p expression and platelet microparticle formation were enhanced. Chronic moderate ethanol consumption improved coronary microcirculation and attenuated ischemia-reperfusion injury. Our results indicate that neutrophil and platelet adhesion molecule expression increases in murine AIDS. Neutrophil and platelet-mediated severe ischemia-reperfusion injury may contribute to increased incidence of cardiomyopathy in AIDS. The cardiovascular protective effects of moderate ethanol consumption may be related to modulation of neutrophil CD11b expression and improve coronary microcirculation. However, chronic ethanol consumption did not preserve myocardial damage by retrovirus infection. In this study, we also demonstrated that vitamin E attenuated AIDS-induced myocardial injury. Vitamin E may be a therapeutic adjuvant agent for preventing and treatment AIDS-induced cardiovascular diseases.