Thermotolerance preserves endothelial vasomotor function during ischemia/reperfusion

Ischemia/reperfusion (I/R) results in endothelial dysfunction, seen as loss of endothelium-dependent vasodilatation. In prolonged ischemia, this can r esult in marked vasospasm or no reflow in the microvasculature. Thermotoler ance (T) attenuates IIR-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 ischem ia/reperfusion group (IIR group) and a group in which thermotolerance (41 /- 0.5 degreesC 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 celia c vascular pedicle for 30 min, followed by 60 min of reperfusion. Vasomotor function [arteriolar constriction:dilatation (C:D) ratio] measured by resp onse to acetylcholine (endothelium-dependent) and sodium nitroprusside (end othelium-independent) and "no-reflow" phenomenon were determined in mesente ric arterioles by intravital microscopy. Data are expressed as means +/- SE M 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 alter ed by I/R. Thermotolerance attenuated this impairment of endothelium-depend ent 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 t hermotolerance preserves endothelial vasomotor function and markedly reduce s "no reflow" in arterioles. (C) 2000 Academic Press.