Sarfeh I J, Tarnawski A
Department of Surgery, Long Beach Veterans Administration Medical Center, CA.
J Clin Gastroenterol. 1991;13 Suppl 1:S18-21. doi: 10.1097/00004836-199112001-00003.
Portal hypertensive gastropathy has recently been recognized as a unique entity distinct from other gastropathies involving the normotensive gastric mucosa. To delineate the pathophysiology of this disorder, we developed a rat model of portal hypertension using two-staged portal vein ligation. In this model, features of the portal hypertensive mucosa include increased luminal hydrogen ion loss, reduced electronegativity of potential difference, and increased submucosal edema. Ultrastructurally, the portal hypertensive gastric mucosa has marked endothelial hypertrophy of capillaries resulting in prominent compromise of microvascular lumina. Combined with the submucosal edema, the microvasculopathy results in reduced oxygenation of the surface gastric mucosa. This is associated with diminished prostaglandin production, which impairs gastric mucosal protection in portal hypertension. These observations are strengthened by experiments that demonstrated significantly increased gastric mucosal damage by alcohol, bile acids, aspirin, and shock/reperfusion in portal hypertensive rats compared to normotensive sham-operated controls. Many of our experimental findings have been confirmed clinically; however, much more research in this area is clearly needed.
门脉高压性胃病最近被确认为一种独特的疾病实体，有别于其他累及血压正常胃黏膜的胃病。为了阐明这种疾病的病理生理学，我们采用两阶段门静脉结扎法建立了门静脉高压大鼠模型。在该模型中，门脉高压黏膜的特征包括管腔内氢离子丢失增加、电位差电负性降低以及黏膜下水肿加重。超微结构上，门脉高压性胃黏膜有明显的毛细血管内皮肥大，导致微血管管腔显著受损。再加上黏膜下水肿，微血管病变导致胃黏膜表面氧合减少。这与前列腺素生成减少有关，后者损害了门脉高压时的胃黏膜保护作用。与血压正常的假手术对照组相比，门脉高压大鼠经酒精、胆汁酸、阿司匹林处理以及经历休克/再灌注后胃黏膜损伤显著增加的实验结果进一步证实了这些观察结果。我们的许多实验发现已得到临床证实；然而，显然该领域还需要更多研究。
