Passive lower limb heat exposure preserved cutaneous microvascular vasodilation following ischemia-reperfusion injury compared to I/R alone (AUC 1.55 vs 0.92 AU), independent of NOS signaling.
Does passive lower limb heat exposure preserve cutaneous microvascular vasodilation following ischemia-reperfusion injury in healthy young adults?
Passive lower limb heating preserves cutaneous microvascular vasodilation following ischemia-reperfusion injury in healthy adults, independent of nitric oxide synthase signaling.
Absolute Event Rate: 1.55% vs 0.92%
Background: Microvascular dysfunction is a hallmark in the progression of chronic disease, with the mechanisms underlying this dysfunction being multi-factorial. Exercise or physical activity is a potent way to enhance vascular function, resulting in improved cardiovascular health. Previous evidence has demonstrated that passive heat therapy (~1°C increase in core temperature) can mimic some of the effects of exercise in large arteries. However, it remains unclear whether passive heating preserves microvascular function, particularly following vascular stress such as ischemia-reperfusion (I/R) injury. We aimed to determine if passive heat exposure maintains cutaneous microvascular responses to the endothelium-dependent agonist acetylcholine (ACh) following I/R injury. We hypothesized that passive heat exposure (42°C, 60-minutes) via lower limb immersion will enhance endothelial-dependent microvascular function and preserve vasodilation in response to vascular injury in vivo. Methods: Ten healthy young adults (18–44 years) completed three study days assessing cutaneous microvascular function via laser Doppler flowmetry and microdialysis. On each day, two microdialysis catheters were inserted subcutaneously and perfused with Ringer’s solution and the nitric oxide synthase inhibitor L-NAME. After trauma hyperemia resolved, ACh dose-response (10-5 –10-1 log M) curves were performed. I/R injury was induced via upper arm cuff inflation (220 mmHg, 20 min) followed by reperfusion (20 min), after which ACh responses were reassessed. On the third day, participants underwent 60 min of lower limb immersion in 42°C water, followed by 1 h recovery, then I/R and ACh dose-response were repeated. Data are presented as area under the curve (AUC) of %CVCmax. Repeated measures ANOVA compared baseline, I/R, and I/R + passive heat responses. Results: AUC responses to ACh were significantly blunted after I/R (Pre: 1.80±0.53 vs. Post I/R: 0.92±0.70 AU, p0.05). At the highest ACh dose (10 - ¹ log M), %CVCmax was reduced after I/R (79.3±20% vs. 32.8±16%, p< 0.05) but maintained following passive heating (Pre I/R: 79.3±20% vs. Post Heat: 78.3±29%, p=0.86). Conclusion: Our data demonstrates that passive lower limb heating preserves microvascular vasodilation despite exposure to vascular stress. However, this preservation is not dependent on intact NOS signaling, as L-NAME had no effect on ACh dilation following post-heat + I/R. These findings support the concept of passive heat therapy’s protective effect on vasodilatory capacity, and suggest this is due to a compensatory vasodilator mechanism. Acknowledgements: Funded by NIA 5T35AG076419-03 (APF), MCW/UWM UREP (JA), AHA 25SURE1512044 (MB), and NHLBI 5R00HL161491-04 (WEH) This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Flynn et al. (Fri,) conducted a other in Healthy (n=10). Passive lower limb heat exposure vs. Ischemia-reperfusion injury without prior heat exposure was evaluated on Cutaneous microvascular responses to acetylcholine (AUC of %CVCmax). Passive lower limb heat exposure preserved cutaneous microvascular vasodilation following ischemia-reperfusion injury compared to I/R alone (AUC 1.55 vs 0.92 AU), independent of NOS signaling.