Tarnawski A S, Sarfeh I J, Stachura J, Hajduczek A, Bui H X, Dabros W, Gergely H
Department of Medicine (Gastroenterology), Veterans Administration Medical Center, Long Beach, California 90822.
Hepatology. 1988 Nov-Dec;8(6):1488-94. doi: 10.1002/hep.1840080604.
Compared with normotensive mucosa, the portal hypertensive gastric mucosa has increased susceptibility to injury by noxious agents such as alcohol and aspirin, but the mechanism of this phenomenon is unclear. Since the microvasculature of the normal gastric mucosa is an important target of injury by these agents, we studied the histologic and ultrastructural features of gastric vasculature and mucosal microvasculature in rats with portal hypertension (produced by staged portal vein ligation) and in sham-operated rats. In portal hypertensive rats, the gastric mucosa was swollen and hyperemic and the endothelial cells of mucosal microvessels had very prominent enlarged cytoplasm obstructing capillary lumina. Quantitative analysis of transmission electron micrographs demonstrated that in portal hypertensive rats the gastric mucosal capillary endothelium had significantly increased cytoplasmic area (236%), increased pinocytic vesicular area (416%) and increased capillary basement membrane thickness (143%) compared to respective parameters in sham-operated control rats. Arterioles in the muscularis mucosae and in submucosa were thickened, and submucosal veins demonstrated features of arterialization. All these findings indicate that portal hypertension produces definite microvascular changes in the gastric mucosa resulting in compromise of the capillary lumina. These changes may be the basis for the observed morphologic and functional abnormalities of the portal hypertensive mucosa and its increased predisposition to injury.
与正常血压的胃黏膜相比，门静脉高压性胃黏膜对酒精和阿司匹林等有害剂损伤的易感性增加，但其机制尚不清楚。由于正常胃黏膜的微血管是这些剂损伤的重要靶点，我们研究了门静脉高压大鼠（通过分期门静脉结扎产生）和假手术大鼠胃血管及黏膜微血管的组织学和超微结构特征。在门静脉高压大鼠中，胃黏膜肿胀、充血，黏膜微血管内皮细胞的细胞质显著肿大，阻塞了毛细血管腔。透射电子显微镜图像的定量分析表明，与假手术对照大鼠的相应参数相比，门静脉高压大鼠胃黏膜毛细血管内皮细胞的细胞质面积显著增加（236%）、吞饮小泡面积增加（416%）以及毛细血管基底膜厚度增加（143%）。黏膜肌层和黏膜下层的小动脉增厚，黏膜下静脉呈现动脉化特征。所有这些发现表明，门静脉高压会在胃黏膜中产生明确的微血管变化，导致毛细血管腔受压。这些变化可能是门静脉高压性胃黏膜所观察到的形态和功能异常及其对损伤易感性增加的基础。
