PLEURAL LIQUID EXCHANGE AND LUNG MECHANICS

描述(改编自申请者的摘要)：长期目标 本研究的目的是确定影响力学性能的因素 胸腔积液交换。这些因素对 对胸腔积液的病因和发病机制的认识 在通风期间对胸膜表面进行有效的润滑。 这项研究集中在两个因素上：通风和微血管 压力。这项建议的第一部分涉及到 胸腔积液滤过通气法。假设是这样的 通过呼吸机增加胸腔积液的滤过率 胸膜/毛细血管膜通透性增加引起的改变 在肺滑动中诱发剪应力。胸腔积液滤过会 在兔子模型中进行测量。埃文的蓝色染色白蛋白将被用作 追踪剂。将使用荧光视频显微镜来测量 伊文氏蓝染色白蛋白的浓度。示踪剂在水中的比例 胸腔积液与血浆中的比值(Cl/Cp)将在几个月内测定 在注入示踪剂之后的时间段以产生氯/Cp随时间的变化 曲线。由呼吸二氧化碳引起的通风增加的影响- 研究了混合空气对氯离子/氯离子浓度随时间的变化曲线。向上的转变 在氯/CP-时间曲线中，随着通气量的增加，将表明 胸膜滤过率和膜通透性均增加。 将使用数学分析来量化这一变化 通风时的过滤速度。以显示 肺滑动速度引起的切应力与胸膜滤过 肺表面速度和胸腔积液的区域变异 在机械通风过程中将测量厚度。被诱导的 肺滑动产生的剪应力，与速度成正比除以 厚度，将与伊文蓝的空间分布相关联 胸壁壁层胸膜中的染料白蛋白。这个 提案的第二部分涉及微血管的影响 胸腔积液交换压力。先前对此进行的研究 实验室研究表明，慢性高血压大鼠(SHR)的 胸膜蛋白浓度和胸膜间隙厚度增加 与正常血压的对照组大鼠相比。这表明自发性高血压病有 更高的毛细压力和更高的过滤速度。为了测试这一点 假设，胸膜毛细血管内的微血管压力将是 用微穿刺法和胸膜滤过率测定 通过埃文的蓝色染色白蛋白从血液中进入 胸膜间隙。

DESCRIPTION (Adapted from the applicant's abstract): The long term goal of this research is to determine the mechanical factors affecting pleural liquid exchange. These factors are important to the understanding of the etiology and pathogenesis of pleural effusions and to the efficient lubrication of the pleural surfaces during ventilation. This research is focused on two factors: ventilation and microvascular pressure. The first part of this proposal concerns the effect of ventilation on pleural liquid filtration. The hypothesis is that ventilation increases the rate of pleural liquid filtration through changes in pleural/capillary membrane permeability caused by increases in lung sliding-induced shear stress. Pleural liquid filtration will be measured in a rabbit model. Evan's blue dyed albumin will be used as the tracer. Fluorescence videomicroscopy will be used to measure the concentration of Evan's blue dyed albumin. The ratio of the tracer in pleural liquid to that in plasma (Cl/Cp) will be measured at several time periods after injection of the tracer to produce a Cl/Cp vs time curve. The effect of increased ventilation caused by breathing a CO2- air mixture on the Cl/Cp vs time curve will be studied. An upward shift in the Cl/Cp vs time curve with increased ventilation will indicate an increase in both the pleural filtration rate and membrane permeability. A mathematical analysis will be used to quantify the change in filtration rate with ventilation. To show the relationship between the lung sliding velocity-induced shear stress and the pleural filtration rate, the regional variation of lung surface velocity and pleural liquid thickness will be measured during mechanical ventilation. The induced shear stress due to lung sliding, proportional to velocity divided by thickness, will be correlated to the spatial distribution of Evan's blue dye albumin in the parietal pleural membrane of the chest wall. The second part of the proposal concerns the effect of microvascular pressure on pleural liquid exchange. A previous study from this laboratory has shown in chronically hypertensive rats (SHR) a decreased pleural protein concentration and an increased pleural space thickness compared to control normotensive rats. This suggests that the SHR has a higher capillary pressure and higher filtration rate. To test this hypothesis, microvascular pressure in pleural capillaries will be measured by the micropuncture technique and the pleural filtration rate by the movement of Evan's blue dyed albumin from the blood into the pleural space.