门脉高压大鼠胃粘膜屏障功能异常的实验研究  

EXPERIMENTAL STUDY ON THE ABNORMAL BARRIER CAPABILITY OF GASTRIC MUCOSA IN PORTAL HYPERTENSIVE RATS

作　　者：周东风[1,2] 孙鹏[1,2] 李红梅 孟茜[1,2] 李兆亭[1,2] 王占民[1,2] 寿楠海 

机构地区：[1]济宁医学院附属医院 [2]山东医科大学附属医院

出　　处：《济宁医学院学报》1998年第4期14-17,共4页Journal of Jining Medical University

摘　　要：目的探讨门脉高压性胃病的发病机理。方法设计两组门脉高压症动物模型，重点观察门脉高压大鼠胃粘膜屏障功能的改变。结果门脉高压大鼠内脏血流量较正常组明显增加（Ｐ＜０００１），而胃粘膜实际处于缺血状态；门脉高压大鼠胃壁结合粘液（ＧＰ）和胃粘膜内源性ＰＧＥ２的含量较对照组显著下降（Ｐ＜００１），而肝硬化大鼠又较单纯门静脉狭窄组更为降低（Ｐ＜００５）；胃基础泌酸量ＢＡＳ三组间无差异，而门脉高压大鼠Ｈ＋返渗量明显高于正常对照组（Ｐ＜０００１），且尤以肝硬化门脉高压大鼠最为显著。结论表明门脉高压大鼠胃粘膜屏障功能遭到严重破坏，尤以肝硬化门脉高压大鼠为甚；门脉高压性胃病的发生与胃粘膜屏障功能严重削弱有关，而非“高酸”所致。Objective To study the pathogeny of portal hypentension gastr opathy.Methods We designed two models of portal hypertensive rats with cirrhosis and extrahepatic portal vein stenosis respectively, and mainly observed the abnormal barrier capability of these two models.Result The splenchic blood flow of the portal hypertensive rats increases, as compared with the control group (P<0 01), but actually gastric mucosa is under the condition of ischmia. Mucus of grastric wall (Glycoprotein, GP) and PGE 2 of gastric mucosa decrease, as compared with the normal control (P<0 01); and more serious decreases occur in cirrhotic portal hypertensive rats. There is no significant difference about the amount of the basal acid secretion among the three groups, but the amount of H + back -diffusion is obviously increased, as compared with the normal control group (P<0 01). The amount of H + BD of cirrhotic portal hypertensive rats is the highest among these three groups.Conclusion The barrier capability of gastric mucosa with portal hypertension is lower than that of the normal contral group and still lower with cirrhotic portal hypertensive rats. The portal hypertensive gastropathy is associated with the lower defense capability not caused by “hyperacid'. The condition of liver function contributes to the changes of barrier capability of gastric mucosa.

关 键 词：肝硬化 门脉高压症 胃粘膜 屏障功能 

分 类 号：R575.202[医药卫生—消化系统]