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.
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Authors | Yinhong Chen, Grace Davis-Gorman, Ronald Ross Watson, Paul F McDonagh |
Journal | Cardiovascular toxicology
(Cardiovasc Toxicol)
Vol. 2
Issue 2
Pg. 119-27
( 2002)
ISSN: 1530-7905 [Print] United States |
PMID | 12271155
(Publication Type: Comparative Study, Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Antioxidants
- CD11b Antigen
- P-Selectin
- Reactive Oxygen Species
- Vitamin E
- N-Formylmethionine Leucyl-Phenylalanine
- Adenosine Diphosphate
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Topics |
- Acquired Immunodeficiency Syndrome
(complications, drug therapy, metabolism)
- Adenosine Diphosphate
(pharmacology)
- Animals
- Antioxidants
(pharmacology)
- CD11b Antigen
(biosynthesis, drug effects)
- Disease Models, Animal
- Female
- Heart Ventricles
(metabolism)
- Mice
- Mice, Inbred C57BL
- Models, Cardiovascular
- Myocardial Infarction
(drug therapy, epidemiology, etiology)
- Myocardial Ischemia
(drug therapy, epidemiology, etiology)
- Myocardial Reperfusion Injury
(complications, drug therapy, metabolism)
- Myocardium
(metabolism, pathology)
- N-Formylmethionine Leucyl-Phenylalanine
(pharmacology)
- Neutrophils
(drug effects, metabolism)
- P-Selectin
(biosynthesis, drug effects)
- Platelet Aggregation
(drug effects)
- Reactive Oxygen Species
(metabolism)
- Risk Factors
- Vitamin E
(pharmacology)
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