title: Vitamin E attenuates myocardial ischemia-reperfusion injury in murine AIDS.
abstract: 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.
authors.affiliation: 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.
authors.forename: Yinhong
authors.initials: Y
authors.lastname: Chen
authors.forename: Grace
authors.initials: G
authors.lastname: Davis-Gorman
authors.forename: Ronald Ross
authors.initials: RR
authors.lastname: Watson
authors.forename: Paul F
authors.initials: PF
authors.lastname: McDonagh
mesh_terms: 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*
chemical_list: D000975:Antioxidants; D039481:CD11b Antigen; D019007:P-Selectin; D017382:Reactive Oxygen Species; D014810:Vitamin E; D009240:N-Formylmethionine Leucyl-Phenylalanine; D000244:Adenosine Diphosphate