Spatiotemporal analysis of the effects of exercise on the hemodynamics of the aorta in hypertensive rats using fluid-structure interaction simulation.

Background and Objective: Hemodynamic changes that lead to increased blood pressure represent the main drivers of organ damage in hypertension. Prolonged increases to blood pressure can lead to vascular remodeling, which also affects vascular hemodynamics during the pathogenesis of hypertension. Exercise is beneficial for relieving hypertension, however the mechanistic link between exercise training and how it influences hemodynamics in the context of hypertension is not well understood. Methods: n exercise model was developed using spontaneously hypertensive rats (SHR) subject to a 12-week treadmill training regime. The heart rates and blood pressures of rats were measured using the tail cuff method, while micro-computed tomography (CT) scanning was used to develop three-dimensional structures of rat aorta, and ultrasound was used to detect rat aortic blood flow and changes to vessel wall structures. Computational fluid dynamics (CFD) and fluid-structure interaction (FSI) models were used to simulate and measure hemodynamic parameters of the rat aortic vessels. In parallel, Masson staining was performed on fixed samples of blood vessels to investigate collagen volume fraction. Hypertensive rats in the sedentary and long-term exercise training groups were subjected to a single bout exercise training, and their aortic hemodynamic parameters were analyzed before, 5 min, 24 h, and 72 h after the single bout exercise. Results: Of the two models, in comparison to actual ultrasonic measurement values recorded, we found that numerical simulation results from the FSI model could more accurately model blood flow in the ascending aorta of hypertensive rats, compared to the CFD model. Moreover, longterm exercise training improved local hemodynamic parameters of blood vessels, and led to improvements in adverse hemodynamic features documented, including time-averaged wall shear stress (TAWSS), oscillatory shear index (OSI), and relative residence time (RRT). Longterm exercise training of SHR also improved local vascular collagen deposition in the aorta, while improvements in vascular remodeling were also correlated with favorable hemodynamic parameters. Compared with sedentary SHR, signals for low TAWSS regions of the aortic arch in SHR on the long-term exercise regime shifted to the position of the ascending aorta after a single bout of exercise. Conclusions: This study demonstrates that FSI is informative to study the spatiotemporal effects of long-term exercise training on hemodynamic changes within the aortas of hypertensive rats, and that long-term exercise is beneficial through its effects to modulate vascular hemodynamics in hypertension.