Pulmonary artery hypertension (PAH) is a complex disorder that can lead to right heart failure. The generation of caveolin-1 deficient mice (CAV-1−/−) has provided an alternative genetic model to study the mechanisms of pulmonary hypertension. However, the vascular adaptations in these mice have not been characterized. To determine the histological and functional changes in the pulmonary and carotid arteries in CAV-1−/− induced PAH. Pulmonary and carotid arteries of young (4–6 months old) and mature (9–12 months old) CAV-1−/− mice were tested and compared to normal wild type mice. Artery stiffness increases in CAV-1−/− mice, especially the circumferential stiffness of the pulmonary arteries. Increases in stiffness were quantified by a decrease in circumferential stretch and transition strain, increases in elastic moduli, and an increase in total strain energy at physiologic strains. Changes in mechanical properties for the pulmonary artery correlated with increased collagen content while changes in the carotid artery correlated with decreased elastin content. We demonstrated that an increase in artery stiffness is associated with CAV-1 deficiency-induced pulmonary hypertension. These results improve our understanding of arterial remodeling in PAH.

中文翻译：

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Caveolin-1 缺乏引起的小鼠肺动脉高压的动脉壁硬化

肺动脉高压 (PAH) 是一种复杂的疾病，可导致右心衰竭。Caveolin-1 缺陷小鼠 (CAV-1-/-) 的产生为研究肺动脉高压的机制提供了另一种遗传模型。然而，这些小鼠的血管适应性尚未得到表征。确定 CAV-1-/- 诱导的 PAH 中肺动脉和颈动脉的组织学和功能变化。测试了年轻（4-6 个月大）和成熟（9-12 个月大）CAV-1-/- 小鼠的肺动脉和颈动脉，并与正常野生型小鼠进行了比较。CAV-1-/- 小鼠的动脉僵硬度增加，尤其是肺动脉的周向僵硬度。刚度的增加通过周向拉伸和过渡应变的减少、弹性模量的增加来量化，以及生理应变下总应变能的增加。肺动脉机械性能的变化与胶原蛋白含量的增加相关，而颈动脉的变化与弹性蛋白含量的降低相关。我们证明了动脉僵硬度的增加与 CAV-1 缺乏引起的肺动脉高压有关。这些结果提高了我们对 PAH 中动脉重塑的理解。