Moreno J, Escobedo D, Calhoun C, Le Saux C Jourdan, Han H C
Department of Mechanical Engineering, University of Texas at San Antonio.
Biomedical Engineering Program, UTSA-UTHSCSA.
Exp Mech. 2021 Jan;6(1):217-228. doi: 10.1007/s11340-020-00666-6. Epub 2020 Oct 14.
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 carotid artery mechanical properties 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 artery remodeling in PAH.
肺动脉高压（PAH）是一种复杂的疾病，可导致右心衰竭。小窝蛋白-1缺陷小鼠（CAV-1）的产生为研究肺动脉高压的机制提供了一种替代遗传模型。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中肺和颈动脉的组织学和功能变化。
对年轻（4-6个月大）和成熟（9-12个月大）的CAV-1小鼠的肺和颈动脉进行检测，并与正常野生型小鼠进行比较。
CAV-1小鼠的动脉僵硬度增加，尤其是肺动脉的周向僵硬度。僵硬度的增加通过周向拉伸和转变应变的降低、弹性模量的增加以及生理应变下总应变能的增加来量化。肺动脉力学性能的变化与胶原蛋白含量的增加相关，而颈动脉力学性能与弹性蛋白含量的降低相关。
我们证明动脉僵硬度增加与CAV-1缺陷诱导的肺动脉高压有关。这些结果增进了我们对PAH中动脉重塑的理解。
