Ethanol modulates coronary permeability to macromolecules in murine aids

被引:2
作者
Chen, YH
Davis-Gorman, G
Watson, RR [1 ]
McDonagh, PF
机构
[1] Univ Arizona, Coll Publ Hlth, Div Hlth Prevent Sci, Sch Med, POB 245155, Tucson, AZ 85724 USA
[2] Univ Arizona, Sch Med, Sarver Heart Ctr, Tucson, AZ 85724 USA
来源
ALCOHOL AND ALCOHOLISM | 2002年 / 37卷 / 06期
关键词
D O I
10.1093/alcalc/37.6.555
中图分类号
R194 [卫生标准、卫生检查、医药管理];
学科分类号
摘要
Background and Aims: The cardiovascular complications of AIDS are serious. However, the underlying mechanisms are unclear. Less is known about how ethanol affects the coronary microcirculation in individuals with AIDS. The aim of this study was to assess the integrity of the coronary microcirculation in murine AIDS mice in the presence or absence of chronic ethanol consumption. Methods: Four groups were studied: control, murine AIDS, ethanol and ethanol plus murine AIDS. Mouse hearts were prepared for direct visualization of the coronary microcirculation and quantification of trans-coronary macromolecular leakage. Hearts were isolated and perfused with diluted rat blood containing fluorescein isothiocyanate-albumin (FITC-BSA). Coronary vessels were observed using intravital fluorescence microscopy after 5, 15 and 25 min of perfusion. The mean luminosity of outside/inside coronary vessels (O/I ratio) was used to quantify FITC-BSA leakage. Results: We found that the mean O/I ratio for the murine AIDS group was significantly greater than in the control group and also significantly increased during the perfusion period. Chronic ethanol consumption did not alter coronary permeability to macromolecules, but improved the coronary haemodynamics in murine AIDS. Conclusions: These findings suggest that murine AIDS impairs the structural and functional coronary endothelium, and moderate ethanol consumption modulates the function of the coronary microcirculation.
引用
收藏
页码:555 / 560
页数:6
相关论文
共 36 条
[1]   Immunologic NO synthase: Elevation in severe AIDS dementia and induction by HIV-1 gp41 [J].
Adamson, DC ;
Wildemann, B ;
Sasaki, M ;
Glass, JD ;
McArthur, JC ;
Christov, VI ;
Dawson, TM ;
Dawson, VL .
SCIENCE, 1996, 274 (5294) :1917-1921
[2]  
Arbabi S, 1999, J IMMUNOL, V162, P7441
[3]   Intensity of myocardial expression of inducible nitric oxide synthase influences the clinical course of human immunodeficiency virus-associated cardiomyopathy [J].
Barbaro, G ;
Di Lorenzo, G ;
Soldini, M ;
Giancaspro, G ;
Grisorio, B ;
Pellicelli, A ;
Barbarini, G .
CIRCULATION, 1999, 100 (09) :933-939
[4]   MODULATION OF TUMOR-NECROSIS-FACTOR AND GAMMA INTERFERON-PRODUCTION BY COCAINE AND MORPHINE IN AGING MICE INFECTED WITH LP-BM5, A MURINE RETROVIRUS [J].
CHEN, GJ ;
WATSON, RR .
JOURNAL OF LEUKOCYTE BIOLOGY, 1991, 50 (04) :349-355
[5]   The effects of HIV infection on endothelial function [J].
Chi, D ;
Henry, J ;
Kelley, J ;
Thorpe, R ;
Smith, JK ;
Krishnaswamy, G .
ENDOTHELIUM-JOURNAL OF ENDOTHELIAL CELL RESEARCH, 2000, 7 (04) :223-242
[6]  
FITZPATRICK DF, 1993, AM J PHYSIOL, V265, pH774
[7]   Increased oxidative stress brought on by pro-inflammatory cytokines in neurodegenerative processes and the protective role of nitrone-based free radical traps [J].
Floyd, RA ;
Hensley, K ;
Jaffery, F ;
Maidt, L ;
Robinson, K ;
Pye, Q ;
Stewart, C .
LIFE SCIENCES, 1999, 65 (18-19) :1893-1899
[8]   PLATELET-ACTIVATING-FACTOR - A CANDIDATE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE 1-INDUCED NEUROTOXIN [J].
GELBARD, HA ;
NOTTET, HSLM ;
SWINDELLS, S ;
JETT, M ;
DZENKO, KA ;
GENIS, P ;
WHITE, R ;
WANG, L ;
CHOI, YB ;
ZHANG, DX ;
LIPTON, SA ;
TOURTELLOTTE, WW ;
EPSTEIN, LG ;
GENDELMAN, HE .
JOURNAL OF VIROLOGY, 1994, 68 (07) :4628-4635
[9]   Retrovirus-elicited interleukin-12 and tumour necrosis factor-alpha as inducers of interferon-gamma-mediated pathology in mouse AIDS [J].
Giese, NA ;
Gazzinelli, RT ;
Actor, JK ;
Morawetz, RA ;
Sarzotti, M ;
Morse, HC .
IMMUNOLOGY, 1996, 87 (03) :467-474
[10]  
Glass JD, 1996, ANNU REV NEUROSCI, V19, P1