Thrombin increases fluid flux in isolated rat lungs by a hemodynamic and not a permeability mechanism.
Thrombin increases fluid flux in isolated rat lungs by a hemodynamic and not a permeability mechanism.
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凝血酶通过血流动力学而非渗透性机制增加离体大鼠肺中的流体通量。
DOI：
10.1152/jappl.1996.80.4.1197
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Minnear,FL
中科院分区：
文献类型：
--
作者：
Waypa,GB;Vincent,PA;Morton,CA;Minnear,FL
α-凝血酶在体外增加内皮蛋白的通透性，并在隔离的灌流肺中诱导体重增加。这项研究的目的是确定凝血酶是否增加了隔离灌流大鼠肺的内皮通透性，以及通透性或血流动力学的变化是否介导了肺重量的增加。通过125I标记的白蛋白清除率与液体流量的回归分析来评估内皮蛋白的通透性，以确定通透性-表面积乘积(PS)和反射系数(Sigma)。凝血酶(5×10(-8)或5×10(-7)M)不改变PS和Sigma控制值的蛋白通透性。凝血酶导致整体血管内液体流量增加，如肺重量增加所示。注射凝血酶后10min，肺动脉压、毛细血管压、动、静脉阻力增加，肺重量因动脉收缩而减轻。在10~50min，压力和阻力下降，但毛细血管压力和静脉阻力下降幅度较小，导致肺重量增加。内皮素受体拮抗剂BQ-123可减轻压力和阻力的持续增加以及肺重量增加的速度。环氧合酶抑制剂吲哚美辛没有作用。这些结果表明，凝血酶诱导的肺重量增加是部分由内皮素介导的毛细血管压力升高所致，而不是由于离体灌流大鼠肺内皮细胞蛋白通透性的增加。
Alpha-Thrombin increases endothelial protein permeability in vitro and induces weight gain in the isolated perfused lung. The objectives of this study were to determine whether thrombin increases endothelial permeability of the isolated perfused rat lung and whether a change in permeability or hemodynamics mediates the gain in lung weight. Endothelial protein permeability was assessed by regression analysis of 125I-labeled albumin clearance vs. fluid flux to determine the permeability-surface area product (PS) and the reflection coefficient (sigma). Thrombin (5 x 10(-8) or 5 x 10(-7) M) did not alter protein permeability from the control values of PS and sigma. Thrombin caused an overall increase in transvascular fluid flux, as depicted by a gain in lung weight. Pulmonary arterial and capillary pressures and arterial and venous resistances increased by 10 min after thrombin injection, and lung weight decreased due to arterial constriction. From 10 to 50 min, pressures and resistances decreased, but capillary pressure and venous resistance decreased to a lesser extent and, as a result, lung weight increased. Pretreatment with BQ-123, an endothelin-receptor antagonist, attenuated the sustained increases in pressures and resistances and the rate of lung weight gain. Indomethacin, a cyclooxygenase inhibitor, had no effect. These findings indicate that the increase in lung weight induced by thrombin results from an elevation of capillary pressure mediated, in part, by endothelin and is not due to an increase in endothelial protein permeability of the isolated perfused rat lung.