Ackerman Z, Karmeli F, Amir G, Rachmilewitz D
Department of Medicine, Hadassah University Hospital, Jerusalem, Israel.
Liver. 1996 Feb;16(1):12-8. doi: 10.1111/j.1600-0676.1996.tb00697.x.
Rats with portal hypertension and experimental liver disease may exhibit increased susceptibility of the gastric mucosa to damage by noxious agents, and increased bacterial translocation through the bowel wall. The aim of this study was to determine mucosal gastric and colonic generation of vasoactive substances, because they may contribute to the altered mucosal function. Rats with partial vein ligation (n = 7), complete bile duct ligation (n = 6) and sham-operated rats (n = 10) were studied. Three weeks following surgery rats were anesthetized, splenic pulp pressure was measured, stomachs and colons were removed and mucosa was extracted for determination of prostaglandin E2, thromboxane B2, leukotriene B4, leukotriene C4 and endothelin-1 by radioimmunoassay (ng/g) and platelet activating factor activity (pg/10 mg) by platelet aggregation. Pulp pressure was > 13 mmHg in partial vein ligated rats and bile duct ligated rats and 6 mmHg in sham-operated rats. No macroscopic or microscopic lesions were seen any of the removed tissues. Gastric mucosal prostaglandin E2 and thromboxane B2 generation were decreased by 35% and 7%, respectively, in bile duct ligated rats (bile duct ligated versus sham-operated, p < 0.05 for prostaglandin E2 and thromboxane B2). Gastric leukotriene B4 and C4 generation, platelet activating factor activity and endothelin-1 content did not differ significantly among the three groups. A different pattern of changes was observed in the colon. Colonic leukotriene B4 generation and endothelin-1 content were increased in bile duct ligated rats by 105% and 210%, respectively (bile duct ligated versus sham-operated, p < 0.05 for leukotriene B4 and endothelin-1). The decreased gastric mucosal prostaglandin E2 generation of bile duct ligated rats may render the gut mucosa of these animals relatively ischemic and vulnerable to damage by noxious agents. The increased colonic leukotriene B4 generation and the increased endothelin-1 content of the colonic mucosa of bile duct ligated rats may promote inflammatory and ischemic changes in the colonic mucosa and may enable bacterial translocation.
患有门静脉高压和实验性肝病的大鼠可能表现出胃黏膜对有害物质损伤的易感性增加，以及细菌通过肠壁的移位增加。本研究的目的是确定胃和结肠黏膜中血管活性物质的生成情况，因为它们可能导致黏膜功能改变。研究对象为部分静脉结扎大鼠（n = 7）、完全胆管结扎大鼠（n = 6）和假手术大鼠（n = 10）。术后三周，将大鼠麻醉，测量脾髓压力，取出胃和结肠，提取黏膜，通过放射免疫测定法（ng/g）测定前列腺素E2、血栓素B2、白三烯B4、白三烯C4和内皮素-1，并通过血小板聚集测定血小板活化因子活性（pg/10 mg）。部分静脉结扎大鼠和胆管结扎大鼠的脾髓压力> 13 mmHg，假手术大鼠为6 mmHg。在所切除的任何组织中均未观察到宏观或微观病变。胆管结扎大鼠的胃黏膜前列腺素E2和血栓素B2生成分别减少了35%和7%（胆管结扎组与假手术组相比，前列腺素E2和血栓素B2的p < 0.05）。三组之间胃白三烯B4和C4生成、血小板活化因子活性和内皮素-1含量无显著差异。在结肠中观察到不同的变化模式。胆管结扎大鼠的结肠白三烯B4生成和内皮素-1含量分别增加了105%和210%（胆管结扎组与假手术组相比，白三烯B4和内皮素-1的p < 0.05）。胆管结扎大鼠胃黏膜前列腺素E2生成减少可能使这些动物的肠道黏膜相对缺血，易受有害物质损伤。胆管结扎大鼠结肠白三烯B4生成增加和结肠黏膜内皮素-1含量增加可能促进结肠黏膜的炎症和缺血性变化，并可能导致细菌移位。
