Vitamin E attenuates myocardial ischemia-reperfusion injury in murine AIDS.
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.
Chen
Yinhong
Y
Divison of Health Prevention Science, College of Public Health and Cardiovascular and Thoracic Surgery and The Sarver Heart Center, School of Medicine, University of Arizona, Tucson, AZ 85724, USA.
Davis-Gorman
Grace
G
Watson
Ronald Ross
RR
McDonagh
Paul F
PF
D000163:Acquired Immunodeficiency Syndrome / Q000150:complications* / Q000188:drug therapy* / Q000378:metabolism; D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D039481:CD11b Antigen / Q000096:biosynthesis / Q000187:drug effects; D004195:Disease Models, Animal; D005260:Female; D006352:Heart Ventricles / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000188:drug therapy / Q000453:epidemiology / Q000209:etiology; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000453:epidemiology / Q000209:etiology*; D015428:Myocardial Reperfusion Injury / Q000150:complications* / Q000188:drug therapy* / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism; D019007:P-Selectin / Q000096:biosynthesis / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism; D012307:Risk Factors; D014810:Vitamin E / Q000494:pharmacology*
D000975:Antioxidants; D039481:CD11b Antigen; D019007:P-Selectin; D017382:Reactive Oxygen Species; D014810:Vitamin E; D009240:N-Formylmethionine Leucyl-Phenylalanine; D000244:Adenosine Diphosphate