Ischemia/reperfusion (I/R) results in endothelial dysfunction, seen as loss of endothelium-dependent vasodilatation. In prolonged ischemia, this can result in marked vasospasm or no reflow in the microvasculature. Thermotolerance (T) attenuates I/R-induced microvascular injury. The aim of this study was to investigate the effect of thermotolerance on I/R-induced vasomotor changes and "no reflow." Sprague-Dawley rats were randomized into an ischemia/reperfusion group (I/R group) and a group in which thermotolerance (41 + 0.5 degrees C for 15 min 18 h prior to I/R) was induced (T + I/R group). IR injury was established by occlusion of the superior mesenteric and celiac vascular pedicle for 30 min, followed by 60 min of reperfusion. Vasomotor function [arteriolar constriction:dilatation (C:D) ratio] measured by response to acetylcholine (endothelium-dependent) and sodium nitroprusside (endothelium-independent) and "no-reflow" phenomenon were determined in mesenteric arterioles by intravital microscopy. Data are expressed as means +/- SEM and were analyzed using ANOVA and chi(2) test. I/R caused a significant decrease in endothelium-dependent vasodilatation (C:D = 1.37+/-0.31 in IR group vs. 2.06+/-0.20 in baseline, P<0.01) and no reflow in arterioles in 16 of 28 unheated rats. Endothelium-independent dilatation was not altered by I/R. Thermotolerance attenuated this impairment of endothelium-dependent dilatation (P<0.01 vs. IR; C:D = 1.95+/-0.19) and reduced no-reflow phenomenon to 4 of 16 rats (P<0.05 vs. IR). This study demonstrated that thermotolerance preserves endothelial vasomotor function and markedly reduces "no reflow" in arterioles.
Copyright 2000 Academic Press.