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

• Published in: Journal of applied physiology (1985) Vol. 134; no. 6; pp. 1364 - 1375
• Main Authors: Hess, Hayden W, Baker, Tyler B, Keeler, Jason M, Freemas, Jessica A, Worley, Morgan L, Johnson, Blair D, Schlader, Zachary J
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.06.2023
• Subjects: Adult; Blood pressure; Erythrocytes; Exocrine glands; Heat stress; Heat tolerance; Heat-Shock Response - physiology; Heating; Hot Temperature; Humans; Hypotheses; In vivo methods and tests; Injuries; Ischemia; Kidneys; Microvasculature; Reabsorption; Renal tubules; Reperfusion; Reperfusion Injury; Skin - blood supply; Sodium; Sweat; Sweat - physiology; Sweat gland; Sweating; Temperature effects; Vasodilation - physiology; ischemia-reperfusion injury; sweat; sweat electrolytes; sweat gland; microvascular function
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00702.2022

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 min of passive heat stress using a water-perfused suit (50°C). At 60 min of whole body heating, one upper arm was occluded for 20 min followed by a 20-min reperfusion. Sweat was collected from each forearm via an absorbent patch pre- and post-I/R. Following the 20-min 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 were 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 ; < 0.01). However, CVC during the local heating was not different between the experimental (80 ± 10% ) and control arms (78 ± 10% ; = 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. In the present study, we have demonstrated that sweat sodium concentration is elevated following ischemia-reperfusion injury during passive heat stress. This does not appear to be mediated by reductions in cutaneous microvascular function or active sweat glands, but may be related to alterations in local sweating responses during heat stress. This study demonstrates a potential use of eccrine sweat glands to understand sodium handling following ischemia-reperfusion injury, particularly given the challenges of in vivo studies of renal ischemia-reperfusion injury in humans.