Cutaneous Microvascular Function Following Ischemia-reperfusion Injury During Passive Heat Stress

Abstract

Increased kidney injury risk during heat stress is mediated, in part, by renal ischemia-reperfusion (IR) injury. However, in vivo studies are not possible in humans. Eccrine sweat glands and the cutaneous circulation have been proposed as a model of the nephron given the physiological similarities (e.g., sodium reabsorption). We previously reported impairments in sweat gland sodium reabsorption following IR injury during passive heat stress, which could be contributed to by alterations in cutaneous microvascular function (i.e., oxygen supply). PURPOSE: Test the hypothesis that forearm cutaneous microvascular function is impaired following IR injury during passive heat stress. METHODS: Fifteen healthy subjects (10 women; age: 25 ± 3 y; body mass index: 23.7 ± 3.5 kg·m2) completed a cross-body design experiment consisting of ~160 min of passive heat stress (core body temperature: +1.5 ± 0.2 °C) utilizing a suit perfused with 50 °C water. At 60 min of whole-body heating, one forearm arm (randomized) was occluded (220 mmHg) for 20 min followed by reperfusion. Local thermal hyperemia tests were performed 20 min following reperfusion using a standard local heating protocol (39 °C for 40 min + 44 °C for 20 min). Forearm skin blood flow was measured continuously at two sites (one heated, one control) on each forearm using laser-Doppler flowmetry. Cutaneous vascular conductance (CVC) was calculated as red blood cell flux/mean arterial pressure (PU/mmHg) and normalized to maximal CVC during local heating to 44 °C. Data are presented as mean ± SD. RESULTS: Maximal CVC was not different between IR and control arms (3.2 ± 0.7 vs. 3.4 ± 0.8 PU/mmHg, respectively; p = 0.48). Approximately 60 min after reperfusion, CVC at the control sites were not different between IR and control arms (78 ± 11 vs. 76 ± 11%, respectively; p = 0.65). Following 40 min of local heating (39 °C), CVC was not different between IR and control arms (80 ± 10 vs. 78 ± 10%, respectively; p = 0.59). CONCLUSION: Cutaneous microvascular function was maintained following IR during passive heat stress indicating that impaired sodium reabsorption is not mediated by reductions in oxygen supply necessary for active transport of sodium. Rather, a disruption in sodium transporter activity may mediate increased sodium excretion, but this remains unknown.