Chronic ethanol consumption exacerbates microcirculatory damage in rat mesentery after reperfusion

Citation
Jy. Han et al., Chronic ethanol consumption exacerbates microcirculatory damage in rat mesentery after reperfusion, AM J P-GAST, 280(5), 2001, pp. G939-G948
Citations number
47
Language
INGLESE
art.tipo
Article
Categorie Soggetti
da verificare
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
ISSN journal
0193-1857 → ACNP
Volume
280
Issue
5
Year of publication
2001
Pages
G939 - G948
Database
ISI
SICI code
0193-1857(200105)280:5<G939:CECEMD>2.0.ZU;2-A
Abstract
Although the negative effect of excessive alcohol consumption on later stre ssful events has long been recognized, pathophysiological mechanisms are in completely understood. We examined possible roles of oxygen radicals and gl utathione content in mesenteric venules of chronically ethanol-fed rats exp osed to ischemia-reperfusion. Changes in microvascular hemodynamics, such a s red blood cell (RBC) velocity, leukocyte adherence, and albumin extravasa tion, were monitored in postcapillary venules by intravital fluorescence mi croscopy. Chronic ethanol feeding significantly exaggerated the magnitude o f the decrease in RBC velocity, the increased number of adherent leukocytes , and increased albumin leakage elicited by 10 min of ischemia followed by 30 min of reperfusion. Oxidative stress in the endothelium of venules monit ored by dihydrorhodamine 123 (DHR) fluorescence was more severe in rats fed ethanol chronically. Both superoxide dismutase and N-acetyl-L-cysteine, wh ich is known to increase glutathione content, reduced the ischemia-reperfus ion-induced decrease in RBC velocity, the number of adherent leukocytes, an d the increase in albumin leakage, as well as oxidative activation of DHR. This suggests that the increased reperfusion-induced microvascular disturba nces in the mesenteric venules of rats fed ethanol chronically are signific antly correlated with excessive production of oxygen-derived free radicals and decreased glutathione synthesis.