Barrios R, Inoue S, Hogg J C
Lab Invest. 1977 Jun;36(6):628-35.
Intercellular junctions in the alveolar epithelium and in the capillary endothelium in lung from five dogs after hemorrhagic shock (mean blood pressure, 40 mm. Hg for 3 hours) and from five control dogs were observed in the electron microscope using the freeze-fracture technique. Following shock zonulae occludentes (tight junctions) in the alveolar epithelium showed alterations in substructure that were not present in control animals. These changes were morphologically similar to those reported in junctions altered after exposure to osmotic gradients with marked degradation and disappearance of junctional strands. The appearance of tight junctions in the capillary endothelium, which were of a rather poorly organized "leaky" type in control animals, was generally unaltered after shock. Disintegration and disappearance of junctional strands in "focal" regions, however, were occasionally observed. The increased pulmonary capillary permeability observed physiologically after hemorrhagic shock could be explained by such alterations of endothelial zonulae occludentes.
采用冷冻断裂技术，在电子显微镜下观察了5只失血性休克犬（平均血压40mmHg，持续3小时）和5只对照犬肺组织中肺泡上皮细胞和毛细血管内皮细胞间的连接。休克后，肺泡上皮细胞中的紧密连接在亚结构上出现了改变，而对照动物中未出现这种情况。这些变化在形态学上与暴露于渗透梯度后连接改变的报道相似，连接条带明显降解和消失。对照动物中毛细血管内皮细胞的紧密连接组织相当疏松，呈“渗漏”型，休克后其外观一般未改变。然而，偶尔会观察到“局部”区域连接条带的解体和消失。失血性休克后生理上观察到的肺毛细血管通透性增加可以用内皮紧密连接的这种改变来解释。
