Shear stress induced by acute heat exposure is not obligatory to protect against endothelial ischemia-reperfusion injury in humans.

Abstract

Acute heat exposure protects against endothelial ischemia-reperfusion (I/R) injury in humans. However, the mechanism/s mediating this protective effect remain unclear. We tested the hypothesis that inhibiting the increase in shear stress induced by acute heat exposure would attenuate the protection of endothelial function following I/R injury. Nine (3 women) young healthy participants were studied under three experimental conditions: 1) thermoneutral control; 2) whole body heat exposure to increase body core temperature by 1.2°C; and 3) heat exposure + brachial artery compression to inhibit the temperature-dependent increase in shear stress. Endothelial function was assessed via brachial artery flow-mediated dilatation before (pre-I/R) and after (post-I/R) 20 min of arm ischemia followed by 20 min of reperfusion. Brachial artery shear rate was increased during heat exposure (681 ± 359 s-1), but not for thermoneutral control (140 ± 63 s-1; P < 0.01 vs. heat exposure) nor for heat + brachial artery compression (139 ± 60 s-1; P < 0.01 vs. heat exposure). Ischemia-reperfusion injury reduced flow-mediated dilatation following thermoneutral control (pre-I/R, 5.5 ± 2.9% vs. post-I/R, 3.8 ± 2.9%; P = 0.06), but was protected following heat exposure (pre-I/R, 5.8 ± 2.9% vs. post-I/R, 6.1 ± 2.9%; P = 0.5) and heat + arterial compression (pre-I/R, 4.4 ± 2.8% vs. post-I/R, 5.8 ± 2.8%; P = 0.1). Contrary to our hypothesis, our findings demonstrate that shear stress induced by acute heat exposure is not obligatory to protect against endothelial I/R injury in humans.NEW & NOTEWORTHY Acute heat exposure protects against endothelial ischemia-reperfusion injury in humans. However, the mechanism/s mediating this protective effect remain unclear. We utilized arterial compression to inhibit the temperature-dependent increase in brachial artery blood velocity that occurs during acute heat exposure to isolate the contribution of shear stress to the protection of endothelial function following ischemia-reperfusion injury. Our findings demonstrate that shear stress induced by acute heat exposure is not obligatory to protect against endothelial I/R injury.