Thermotolerance preserves endothelial vasomotor function during ischemia/reperfusion.

摘要: Ischemia/reperfusion (I/R) results in endothelial dysfunction, seen as loss of endothelium-dependent vasodilatation. In prolonged ischemia, this can result marked vasospasm or no reflow the microvasculature. Thermotolerance (T) attenuates I/R-induced microvascular injury. The aim study was to investigate effect thermotolerance on vasomotor changes and “no reflow.” Sprague–Dawley rats were randomized into an ischemia/reperfusion group (I/R group) a which (41 + 0.5°C for 15 min 18 h prior I/R) induced (T I/R group). IR injury established by occlusion superior mesenteric celiac vascular pedicle 30 min, followed 60 reperfusion. Vasomotor function [arteriolar constriction:dilatation (C:D) ratio] measured response acetylcholine (endothelium-dependent) sodium nitroprusside (endothelium-independent) “no-reflow” phenomenon determined arterioles intravital microscopy. Data are expressed means ± SEM analyzed using ANOVA χ2 test. caused significant decrease vasodilatation (C:D = 1.37 0.31 vs 2.06 0.20 baseline, P < 0.01) 16 28 unheated rats. Endothelium-independent dilatation not altered I/R. attenuated impairment (P 0.01 IR; C:D 1.95 0.19) reduced no-reflow 4 0.05 IR). This demonstrated that preserves markedly reduces reflow” arterioles.