Elevations in sweat sodium concentration following ischemia-reperfusion injury during passive heat stress

Renal ischemia-reperfusion (I/R) injury results in damage to the renal tubules and causes impairments in sodium [Na+] reabsorption. Given the inability to conduct mechanistic renal I/R injury studies in vivo in humans, eccrine sweat glands have been proposed as a surrogate model given the anatomical and physiological similarities. We tested the hypothesis that sweat Na+ concentration is elevated following I/R injury during passive heat stress. We also tested the hypothesis that I/R injury during heat stress will impair cutaneous microvascular function. Fifteen young healthy adults completed ~160 minutes of passive heat stress utilizing a water-perfused suit (50°C). At 60 minutes of whole-body heating, one upper arm was occluded for 20 minutes followed by a 20-minute reperfusion. Sweat was collected from each forearm pre and post I/R. Following the 20-minute reperfusion, cutaneous microvascular function was measured via local heating protocol. Cutaneous vascular conductance (CVC) was calculated as red blood cell flux/mean arterial pressure and normalized to CVC during local heating to 44°C. Na+ concentration was log transformed and data reported as a mean change from pre I/R (95% confidence interval). Changes in sweat sodium concentration from pre I/R differed between arms post I/R (Experimental Arm: +0.97 [+0.67 - 1.27] [LOG] Na+; Control Arm: +0.68 [+0.38 - 0.99] [LOG] Na+; p<0.01). However, CVC during the local heating was not different between the experimental (80±10%max) and control arms (78±10%max; p=0.59). In support of our hypothesis, Na+ concentration was elevated following I/R injury, but likely not accompanied by alterations in cutaneous microvascular function.