Pulmonary arterial smooth muscle contractility in hypoxia-induced pulmonary hypertension.
Pulmonary arterial smooth muscle contractility in hypoxia-induced pulmonary hypertension.
复制标题
缺氧引起的肺动脉高压中的肺动脉平滑肌收缩力。
DOI：
10.1152/jappl.1994.77.1.406
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Packer,CS
中科院分区：
文献类型：
--
作者：
Griffith,SL;Rhoades,RA;Packer,CS
高顺应性低阻力肺血管系统在慢性低氧条件下发生明显改变。低氧和/或高血压引起的重塑包括平滑肌肥大和增生以及结缔组织的过度沉积，这可能有助于维持或加剧本已升高的肺动脉(PA)压力。本研究的目的是探讨慢性低氧对血管平滑肌收缩特性的影响。在低氧14天诱导的大鼠肺动脉高压模型上，进行了等长和等张实验。在缺氧性肺动脉高压的发展过程中，血管壁厚度增加了一倍。在功能上，等轴应力(力与横截面面积之比)有所下降。短缩速度和总短缩能力无明显差异。本研究提供的证据表明，在缺氧性肺动脉高压的发生和/或维持过程中，PA平滑肌收缩功能的改变除了在形态上的改变外，似乎也起着一定的作用。
The highly compliant low-resistance pulmonary vasculature is markedly altered with chronic hypoxia. Remodeling in response to hypoxia and/or hypertension involves hypertrophy and hyperplasia of smooth muscle and excessive deposition of connective tissue that likely contributes to the maintenance or exasperates the already elevated pulmonary arterial (PA) pressure. The purpose of this study was to investigate the effect of chronic hypoxia on the contractile properties of PA smooth muscle. Isometric and isotonic experiments were performed on excised PA rings from pulmonary hypertensive (induced by 14 days of hypoxia) Sprague-Dawley rats. A doubling of the vessel wall thickness occurred during the development of hypoxia-induced pulmonary hypertension. Functionally, there was a decrease in isometric stress (force to cross-sectional area ratio). No difference was detected in the velocity of shortening or in total shortening ability. This study provides evidence that, in addition to the morphological changes, changes in PA smooth muscle contractility also appear to play a role in the development and/or maintenance of hypoxia-induced pulmonary hypertension.