MECHANICS OF PULMONARY VASCULAR SMOOTH MUSCLE

本提案的长期目标是了解 发生在肺血管平滑肌的功能 高血压（PH）。 隔震混凝土的基本力学性能 血管将在正常大鼠和肺动脉高压大鼠中进行研究。 长期暴露在低压缺氧环境中引起的高血压。 低氧诱导的PH的特征是广泛的血管 重塑包括平滑肌量增加， 肌肉向周围延伸， 组织. 增加的阻力是增加的被动 壁僵硬和平滑肌收缩功能改变。 该建议将描述光滑的性质 正常肺动、静脉血管肌细胞 高血压大鼠 周长：张力和力： 速度关系将被确定并与 收缩蛋白含量和形态特征。 将确定最大主动应力，并将其与 肌动蛋白和肌球蛋白的量。 这一基本特征将是 在动脉和动脉的大小血管上完成， 静脉系统 此外，单肺血管通畅 肌肉细胞将被分离并独立于血管进行研究 壁和周围细胞。 药物依赖性 将评估圆周上肺血管的反应。 该提案将提供有关财产的独特数据 肺血管平滑肌在正常以及 高血压血管床 这种类型的特征将 深入了解这种循环的功能和变化 导致肺动脉高压的发生

The long term goal of this proposal is to understand changes that occur in the function of vascular smooth muscle in pulmonary hypertension (PH). The basic mechanical properties of isolated vessels will be studied in normal rats and those with pulmonary hypertension induced by chronic exposure to hypobaric hypoxia. Hypoxic induced PH is characterized by extensive vascular remodeling including increased amounts of smooth muscle, extension of that muscle peripherally and increases in connective tissue. The increased resistance is a function of increased passive wall stiffness and altered smooth muscle contractile function. This proposal will characterize the properties of the smooth muscle cells of pulmonary arterial and venous vessels from normal and hypertensive rats. Circumference: tension and force: velocity relationships will be determined and related to contractile protein content and morphologic characteristics. Maximal active stress will be determined and related to the amount of actin and myosin. This basic characterization will be completed on large and small vessels from both arterial and venous system. In addition, single pulmonary vascular smooth muscle cells will be isolated and studied independent of the vessel wall and surrounding cells. The dependence of pharmacologic response of pulmonary vessels on circumference will be assessed. This proposal will provide unique data concerning the properties of pulmonary vascular smooth muscle in the normal as well as hypertensive vascular bed. This type of characterization will provide insight into the function of this circulation and changes responsible for the development of pulmonary hypertension.