PLEURAL LIQUID EXCHANGE AND LUNG MECHANICS

描述（改编自申请人的摘要）：长期目标 这项研究的目的是确定影响 胸膜液交换 这些因素对 了解胸腔积液的病因和发病机制， 在通气期间胸膜表面的有效润滑。 本研究集中在两个因素：通气和微血管 压力 本建议的第一部分是关于 胸腔液体过滤通气。 前提是 通气增加胸膜液体滤过率， 胸膜/毛细血管膜通透性增加引起的变化 肺滑动引起的剪切应力。 胸膜液过滤将 在兔子模型中测量。 埃文的蓝色染色白蛋白将被用作 追踪器 荧光视频显微镜将用于测量 埃文蓝染白蛋白的浓度。 示踪剂在 将在几个时间点测量胸膜液与血浆中的比率（Cl/Cp） 注入示踪剂后的时间段，以产生Cl/Cp vs时间 曲线 呼吸二氧化碳引起的通气量增加的影响- 空气混合物的Cl/Cp随时间的变化曲线将被研究。 向上偏移 在增加通气量的Cl/Cp vs时间曲线中， 胸膜滤过率和膜通透性增加。 将使用数学分析来量化 通气时的滤过率 为了展示 肺滑动速度引起的切应力与胸膜滤过 率、肺表面速度和胸腔积液的区域性变化 将在机械通气期间测量厚度。 感应 肺滑动产生的剪切应力，与速度除以 厚度，将与伊文思蓝的空间分布相关 在胸壁的壁胸膜中染色白蛋白。 的 建议的第二部分涉及微血管的影响， 胸膜液体交换压力。 此前的一项研究表明， 实验表明，在慢性高血压大鼠（SHR）中， 胸膜蛋白浓度和胸膜间隙厚度增加 与对照组血压正常的大鼠相比。 这表明SHR具有 更高的毛细管压力和更高的过滤速率。 为了验证这一 假设，胸膜毛细血管中的微血管压将 通过微穿刺技术和胸膜滤过率测量 通过埃文的蓝色染色白蛋白从血液进入血液的运动， 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.