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为观察门静脉高压时胃粘膜的屏障功能，研究设计肝硬化和肝外门静脉狭窄两组门静脉高压动物模型，观察其胃粘膜屏障功能的变化并与正常对照组对比研究。结果显示：门静脉高压大鼠内脏血流量明显增加，而胃粘膜实际处于局部缺血状态；胃壁结合粘液量（ＧＰ）和胃粘膜ＰＧＥ２含量较对照组显著降低，尤以肝硬化门静脉高压大鼠为甚；胃基础泌酸量（ＢＡＳ）三组间无差异，而门静脉高压大鼠Ｈ＋返流量（Ｈ＋ＢＤ）明显高于对照组，以肝硬化大鼠最为显著。结果表明：门静脉高压性胃病（ＰＨＧ）的发生与胃粘膜屏障功能严重削弱有关；而非“高酸”所致；肝功能受损参与胃粘膜病变的发生。
To observe the barrier function of gastric mucosa in patients with portal hypertension, we designed two models of portal hypertension in animal models of liver cirrhosis and extrahepatic portal vein stenosis. The changes of gastric mucosal barrier function were observed and compared with the normal control group. The results showed that visceral blood flow in portal hypertensive rats increased significantly, while the gastric mucosa was actually ischemic. The content of gastric mucosal mucosa (GP) and PGE2 in gastric mucosa decreased significantly, especially in cirrhotic rats with portal hypertension (BAS) no difference between the three groups, while portal hypertensive rats H + regurgitation (H + BD) was significantly higher than the control group, the most significant in cirrhotic rats. The results showed that: the occurrence of portal hypertensive gastropathy (PHG) is related to the severe impairment of gastric mucosal barrier function; not caused by “high acid”; impaired liver function is involved in the occurrence of gastric mucosal lesions.