INDUCTION OF HEAT-SHOCK-PROTEIN 72KDA EXPRESSION IS ASSOCIATED WITH ATTENUATION OF ISCHEMIA-REPERFUSION INDUCED MICROVASCULAR INJURY

Leukocyte-endothelial interaction is a pivotal step in the pathogenesi s of ischemia-reperfusion (I/R) injury. Exposure of cells to a subcrit ical heat stress may protect cells from subsequent I/R injury, through induction of a 72-kDa heat shock protein (HSP72). The aim of this stu dy was to investigate the effect of thermotolerance on leukocyte adher ence and migration during an I/R period in rat mesenteric postcapillar y venules. Sprague-Dawley rats mere randomized into control (sham I/R) , I/R, and thermotolerance + I/R groups. Thermotolerance was induced 1 8 hr prior to I/R, which was in turn established by occlusion of the s uperior mesenteric vascular pedicle for 10 mins, followed by 60 mins o f reperfusion. The blood flow, leukocyte rolling velocity, and the num ber of adherent and migrated leukocytes in postcapillary venules were measured by intravital microscopy. I/R significantly decreased the rol ling velocity of leukocytes; increased the number of adherent leukocyt es at 10, 30, and 60 mins after reperfusion; and also increased the nu mber of migrated leukocytes at 60 mins after reperfusion. Thermotolera nce induction expression of HSP72 in pulmonary, intestinal, and mesent eric tissues was determined by Western immunoblotting. Thermotolerance significantly prevented the I/R-induced decrease in rolling velocity of leukocytes, the increase in the number of adherent leukocytes at 30 and 60 mins, and the increase in the number of migrated leukocytes at 60 mins. This results suggest that thermotolerance attenuates I/R inj ury by modulating leukocyte-endothelial interaction in vivo possibly b y increasing tissue expression of HSP72. (C) 1997 Academic Press.