Non-pharmacological modulation of aortic hemodynamic condition by extreme heat.

Abstract

Extreme heat exposure is a promising non-pharmacological strategy for cardiovascular health, yet its underlying hemodynamic mechanisms remain poorly understood. Here, computational fluid dynamics (CFD) was used to assess heat-induced changes in aortic blood flow. Three-dimensional aortic geometries were reconstructed from computed tomography scans of six healthy adults (mean age: 50.8 ± 12.8  years). Inlet conditions were adjusted to simulate thermal stress (80-100 °C) based on reported increases in cardiac output (67%) and heart rate (33%), whereas outlet boundaries were modeled using Windkessel elements with parameters tuned for flow redistribution. The effects of vascular deformation were accounted for using a fluid-structure interaction approach. Key hemodynamic metrics, including time-averaged wall shear stress (TAWSS), oscillatory shear index (OSI), relative residence time (RRT), and endothelial cell activation potential (ECAP), were quantified before and after heat exposure. In parallel, 12 rats were randomly assigned to a heat-exposed group (n = 6; 41 °C, 20  min) or a control group (n = 6; 24 °C, 20  min), after which the abdominal aorta was harvested for immunofluorescence analysis of eNOS expression. Wall shear stress increased by at least 89.9% throughout the aorta and across the cardiac cycle, with the greatest increase observed at the aortic arch. TAWSS exhibited an inverse "S"-shaped spatial distribution, with regions of higher baseline shear showing greater amplification. In contrast, OSI and RRT decreased during heat exposure. On average, TAWSS rose by 108.5%, whereas OSI and RRT fell by 22.5% and 56.5%, respectively. eNOS expression in rat aortas was significantly higher in the heat-exposed group than in the control group (P < 0.05). Additionally, ECAP decreased by 57.1% during heat exposure. These results demonstrate that heat exposure significantly enhances aortic hemodynamics and may serve as a non-pharmacological strategy to improve arterial function, offering a potential alternative for individuals unable to exercise.