Koch T, Duncker H P, Rosenkranz S, Neuhof H, Van Ackern K
Department of Anaesthesiology, Faculty for Clinical Medicine Mannheim, University of Heidelberg, Federal Republic of Germany.
J Appl Physiol (1985). 1992 Dec;73(6):2396-402. doi: 10.1152/jappl.1992.73.6.2396.
Different pathomechanisms in the development of pulmonary edema are being discussed. We investigated the effect of pathogenetically varying forms of edema on lung vascular barrier function in isolated cell-free perfused rabbit lungs. As an index of permeability, capillary filtration coefficients (Kfc) were determined from the slope of lung weight change over periods of stepwise venous pressure elevation (5, 7.5, and 10 mmHg) before (controls) and 60 min after edema induction. Edema was induced by venous congestion (n = 6), by application of arachidonic acid in the presence of diclofenac sodium (n = 6), and by elastase application (n = 6). Control values ranged from 0.28 to 0.51 ml.min-1 x mmHg-1 x 100 g-1. Kfc was significantly enhanced after edema induction up to 243% of control value in the hydrostatic edema, 357% in the arachidonic acid edema, and 594% in the elastase edema. When the alterations in capillary filtration due to the different types of edema were compared, Kfc was significantly higher in the proteinase edema, indicating an irreversibly damaged barrier function. These data exemplify different pathophysiological characteristics due to the pathogenesis of interstitial edema formation.
目前正在讨论肺水肿发展过程中的不同病理机制。我们研究了不同发病机制形式的水肿对离体无细胞灌注兔肺血管屏障功能的影响。作为通透性指标，在水肿诱导前（对照组）以及诱导后60分钟，通过逐步升高静脉压（5、7.5和10 mmHg）期间肺重量变化的斜率来测定毛细血管滤过系数（Kfc）。通过静脉淤血（n = 6）、在双氯芬酸钠存在下应用花生四烯酸（n = 6）以及应用弹性蛋白酶（n = 6）来诱导水肿。对照值范围为0.28至0.51 ml·min-1·mmHg-1·100 g-1。水肿诱导后，Kfc显著升高，在静水压性水肿中高达对照值的243%，在花生四烯酸性水肿中为357%，在弹性蛋白酶性水肿中为594%。当比较不同类型水肿引起的毛细血管滤过变化时，蛋白酶性水肿中的Kfc显著更高，表明屏障功能受到不可逆损伤。这些数据例证了间质性水肿形成机制导致的不同病理生理特征。
