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

Persistent Link:
http://hdl.handle.net/10150/289750
Title:
The effects of murine AIDS and ethanol consumption on the severity of myocardial ischemic injury
Author:
Chen, Yinhong
Issue Date:
2001
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
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.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Health Sciences, Nutrition.; Health Sciences, Pathology.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Graduate College; Nutritional Sciences
Degree Grantor:
University of Arizona
Advisor:
Watson, Ronald R.

Full metadata record

DC FieldValue Language
dc.language.isoen_USen_US
dc.titleThe effects of murine AIDS and ethanol consumption on the severity of myocardial ischemic injuryen_US
dc.creatorChen, Yinhongen_US
dc.contributor.authorChen, Yinhongen_US
dc.date.issued2001en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractCardiovascular 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.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectHealth Sciences, Nutrition.en_US
dc.subjectHealth Sciences, Pathology.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplineNutritional Sciencesen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorWatson, Ronald R.en_US
dc.identifier.proquest3040116en_US
dc.identifier.bibrecord.b42455595en_US
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