Bachofen H, Schürch S, Michel R P, Weibel E R
Department of Anatomy, University of Berne, Switzerland.
Am Rev Respir Dis. 1993 Apr;147(4):989-96. doi: 10.1164/ajrccm/147.4.989.
To study the accumulation and distribution of edema fluid and the associated changes in alveolar microarchitecture, edema was induced in excised rabbit lungs perfused with 6% albumin solution. The lungs, including the edema fluid, were then fixed by vascular perfusion with glutaraldehyde, osmium tetroxide, and uranyl acetate. Tissue samples were analyzed by light microscopy and transmission and scanning electron microscopy. We found (1) fixation was successful in that the albumin in the edema fluid formed coherent webs indicating the location and arrangement of the extravascular fluid accumulations; (2) regardless of the filtration pressure (about 29 mm Hg in one set of experiments and about 14 mm Hg in the other), an apical to basal gradient of fluid accumulation was found. This gradient was absent in lungs held in the inverse position, suggesting that the regional distribution of pulmonary edema is not simply gravity dependent. At the same lung height, there was a remarkable inhomogeneity of interstitial and alveolar edema. (3) Both the inhomogeneous distribution of fluid and the resulting changes in surface tension affected the entire alveolar architecture. (4) Within interstitial and alveolar spaces, there were striking inequalities in the density of the proteinaceous fluid pools that suggest local differences in the sieving properties of the barriers, that is, in the reflection coefficients for albumin. In conclusion, our findings suggest that the formation of pulmonary edema cannot be explained solely by uniform membrane models for fluid exchange.
为研究水肿液的蓄积与分布以及肺泡微结构的相关变化,我们对用6%白蛋白溶液灌注的离体兔肺诱导产生水肿。然后,通过用戊二醛、四氧化锇和醋酸铀进行血管灌注,将包括水肿液在内的肺固定。组织样本通过光学显微镜、透射电子显微镜和扫描电子显微镜进行分析。我们发现:(1)固定是成功的,因为水肿液中的白蛋白形成了连贯的网,表明血管外液体积聚的位置和排列;(2)无论滤过压如何(一组实验中约为29 mmHg,另一组中约为14 mmHg),均发现液体蓄积存在从顶端到基底的梯度。在倒置位置的肺中不存在这种梯度,这表明肺水肿的区域分布并非简单地依赖于重力。在相同的肺高度,间质和肺泡水肿存在显著的不均匀性。(3)液体的不均匀分布以及由此产生的表面张力变化影响了整个肺泡结构。(4)在间质和肺泡间隙内,蛋白质液体池的密度存在显著差异,这表明屏障的筛分特性存在局部差异,即白蛋白的反射系数存在差异。总之,我们的研究结果表明,肺水肿的形成不能仅用统一的液体交换膜模型来解释。