MECHANICS OF PULMONARY VASCULAR SMOOTH MUSCLE

这项提案的长期目标是了解 发生在肺血管平滑肌功能中 高血压(PH)。隔热材料的基本力学性能 血管将在正常大鼠和那些患有肺病的大鼠身上进行研究 慢性暴露在低压低氧环境下引起的高血压。 低氧性肺动脉高压的特点是广泛的血管 重塑包括增加大量的平滑肌， 肌肉向外延伸并增加结缔组织 组织。增加的阻力是被动增加的函数 室壁僵硬和血管收缩功能改变。 这一提议将描述光滑性的性质 正常肺动、静脉血管的肌细胞 和高血压大鼠。周长：张力和力： 速度关系将被确定并与 收缩蛋白含量及形态特征。 最大活动应力将被确定，并与 肌动蛋白和肌球蛋白的含量。这一基本特征将是 在大小血管上完成，从动脉和 静脉系统。此外，单个肺血管通畅 肌肉细胞将被分离并独立于血管进行研究 墙和周围的细胞。药理依赖 将评估肺血管对周长的反应。 该提案将提供有关物业的唯一数据 正常肺血管和正常肺血管内皮细胞 高血压血管床。这种类型的特征将 提供对这种循环和变化的功能的洞察 对肺动脉高压的发展负责。

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.