Shumko J Z, DeFouw D O
Department of Anatomy, UMDNJ-New Jersey Medical School, Newark 07103.
Histol Histopathol. 1987 Jan;2(1):79-87.
The principal focus of this study was to evaluate the hypothesis that increased interstitial fluid pressures served to stimulate de novo vesicle formation in pulmonary capillary endothelium. Direct measurements of interstitial fluid pressures within the alveolar septa pose great technical difficulty. The pleural space and subpleural capillaries are easily accessible, and thus, provide a more feasible model to test this hypothesis. After hydrostatic pressure of pleural space fluid was increased by periodic saline infusions into the pleural cavity, vesicle numerical densities were significantly increased in portions of the subpleural capillary endothelium. Those segments of the endothelium that directly apposed the interstitium of the visceral pleura displayed de novo vesicle formation. The endothelial segments located immediately adjacent to the alveolar epithelium were not affected by the elevated interstitial fluid pressures. In addition to the increased vesiculation, those same segments of the endothelium were characterized by increased attenuation of their cytoplasmic compartments. These conformational changes in the plasmalemma of portions of the subpleural capillary endothelium provide support to the tentative hypothesis, however, whether the increased numbers of vesicles contribute to a potential transendothelial transport system or expand a possible static network of membrane invaginations remains uncertain.
肺泡间隔内间质液压力升高会刺激肺毛细血管内皮细胞重新形成囊泡。直接测量肺泡间隔内的间质液压力存在很大的技术困难。胸膜腔和胸膜下毛细血管易于接近，因此，提供了一个更可行的模型来检验这一假设。通过定期向胸膜腔内注入生理盐水来增加胸膜腔液的静水压力后，胸膜下毛细血管内皮细胞部分的囊泡数量密度显著增加。直接与脏层胸膜间质相邻的内皮细胞段出现了新的囊泡形成。紧邻肺泡上皮的内皮细胞段不受间质液压力升高的影响。除了囊泡形成增加外，这些相同的内皮细胞段的细胞质区室衰减也增加。胸膜下毛细血管内皮细胞部分质膜的这些构象变化为这一初步假设提供了支持，然而，囊泡数量的增加是否有助于潜在的跨内皮运输系统或扩展可能的膜内陷静态网络仍不确定。
