门脉高压时胃粘膜病变发生机制的实验研究

Pathogenesis of gastric mucosal lesions in portal hypertension

为探讨门脉高压时胃粘膜膜病变的发生机制，本文对四氯化碳所致的肝硬变伴门脉高压大鼠的胃粘膜主要防御和损伤因子进行了测定，并观察了胃粘膜超微结构。结果表明，门脉高压大鼠的胃粘膜前列腺素Ｅ＿２风含量、胃粘膜血流量和胃壁结合粘膜量明显低于正常大鼠（均为Ｐ＜０．００１），而胃腋ｐＨ值，胃酸浓度、胃酸分泌量和胃蛋白酶活性与正常比较无明显差异（均为Ｐ＞０．０５）。门脉高压大鼠的胃粘膜毛细血管组织结构的完整性破坏，毛细血管内血液淤滞。上皮细胞和壁细胞变形，细胞器破坏，细胞处于低功能状态。显示，胃粘膜防御机制的削弱是门脉高压时胃粘膜病变发生的主要因素。

Gastric mucosal prostaglandin E_2 content (PGE_2), gastric mucosal blood flow(GMBF), gastric adherent mucus(GAM), pH of gastric Juice, gastric acid concentra- tion(GAC), gastric acid output(GAO)and pepsin activity(AP)were determined. Ultras- tructure of gastric mucosa was observed in the CCl-induced liver cirrhosis in rats with portal hypertension. The aim was to study the pathogenesis of portal hypertensive gastric mucosal lesions. In the portal hypertensive rats, PGE_2,GMBF and GAM were significan- tly lower than those of normal rats(P<0.001); pH of gastric juice, GAC, GAO and AP were similar to normal rats(P>0.05). The integrity of capillaries in gastric mucosa was damaged, blood was accumulated and detained in capillaries; the secretory function was im- paired and organelles were damaged in epithelial and parietal cells. The above data indicatedthat the pathogensis of portal hypertensive gastric mucosal lesions was due to weakeningof gastric mucosal protective mechanism.