Pulmonary arterial hypertension (PAH) is associated with elevated pulmonary arterial pressure. PAH prognosis remains poor with a 15% mortality rate within 1 year, even with modern clinical management. Previous clinical studies proposed wall shear stress (WSS) to be an important hemodynamic factor affecting cell mechanotransduction, growth and remodeling, and disease progress in PAH. However, WSS in vivo is typically at most 2.5 Pa and a doubt has been cast whether WSS alone can drive disease progress. Furthermore, our current understanding of PAH pathology largely comes from small animals' studies in which caliber enlargement, a hallmark of PAH in humans, is rarely reported. Therefore, a large‐animal experiment on pulmonary arteries (PAs) is needed to validate whether increased pressure can induce enlargement of PAs caliber. In this study, we use an inflation testing device to characterize the mechanical behavior, both nonlinear elastic behavior and irreversible damage of porcine arteries. The parameters of elastic behavior are estimated from the inflation test at a low‐pressure range before and after over‐pressurization. Then, histological images are qualitatively examined for medial and adventitial layers. This study sheds light on the relevance of pressure‐induced damage mechanism in human PAH.

中文翻译：

---

肺动脉高压的潜在损害：压力性肺动脉损伤的实验研究

肺动脉高压（PAH）与肺动脉压升高有关。即使采用现代临床管理，PAH 的预后仍然很差，1 年内死亡率为 15%。先前的临床研究提出壁剪切应力 (WSS) 是影响 PAH 细胞机械传导、生长和重塑以及疾病进展的重要血流动力学因素。然而，体内的 WSS 通常最多为 2.5 Pa，并且有人怀疑单独的 WSS 是否可以推动疾病进展。此外，我们目前对 PAH 病理学的理解主要来自对小动物的研究，其中很少报道口径扩大（人类 PAH 的标志）。因此，需要对肺动脉（PAs）进行大型动物实验来验证增加的压力是否会导致PAs口径扩大。在这项研究中，我们使用充气测试设备来表征猪动脉的机械行为，包括非线性弹性行为和不可逆损伤。弹性行为的参数是通过在过压前后的低压范围内的充气试验来估计的。然后，定性检查组织学图像的内侧和外膜层。本研究揭示了压力诱导损伤机制在人类 PAH 中的相关性。