摘要
Abstract Objective To investigate the pathogenetic role of endogenous angiotensin Ⅱ (AngⅡ) in the mechanism of stress ulcer in obstructive jaundice rats and to detect the effect of angiotensin converting enzyme inhibitor (ACEI) on stress ulcer in obstructive jaundice rats. Methods After common bile duct ligation (CBDL) in Wistar rats, the content of plasma and gastric mucosal AngⅡ, gastric mucosal blood flow (GMBF) and gastric mucosal damage were measured, and the relationship among them was analyzed. Results The plasma AngⅡ contents increased much more significantly at 1, 3, 7 and 14 days following CBDL than those in non CBDL rats (P<0.05, <0.01, <0.01 and <0.01, respectively). Within 120 minutes following cold restraint stress, plasma and gastric mucosal AngⅡ contents were elevated, GMBF decreased, and ulcer index and gastric mucosal damage increased more significantly than those in non cold restraint stress rats (P<0.05, <0.05, <0.01, <0.01 and <0.05, respectively). Administration of an ACEI, enalaprili, to CBDL rats (5 mg·kg -1 ·day -1 , orally for two days) before stress reduced both the plasma and gastric mucosal AngⅡ levels, inhibited the decrease of GMBF and decreased ulcer index and gastric mucosal damage (P<0.001, <0.01, <0.01, <0.01 and <0.05, respectively). Conclusion The endogenous AngⅡ plays a significant pathogenetic role in the development of stress ulcer in obstructive jaundice rats, and ACEI may prevent stress ulcer.
Abstract Objective To investigate the pathogenetic role of endogenous angiotensin Ⅱ (AngⅡ) in the mechanism of stress ulcer in obstructive jaundice rats and to detect the effect of angiotensin converting enzyme inhibitor (ACEI) on stress ulcer in obstructive jaundice rats. Methods After common bile duct ligation (CBDL) in Wistar rats, the content of plasma and gastric mucosal AngⅡ, gastric mucosal blood flow (GMBF) and gastric mucosal damage were measured, and the relationship among them was analyzed. Results The plasma AngⅡ contents increased much more significantly at 1, 3, 7 and 14 days following CBDL than those in non CBDL rats (P<0.05, <0.01, <0.01 and <0.01, respectively). Within 120 minutes following cold restraint stress, plasma and gastric mucosal AngⅡ contents were elevated, GMBF decreased, and ulcer index and gastric mucosal damage increased more significantly than those in non cold restraint stress rats (P<0.05, <0.05, <0.01, <0.01 and <0.05, respectively). Administration of an ACEI, enalaprili, to CBDL rats (5 mg·kg -1 ·day -1 , orally for two days) before stress reduced both the plasma and gastric mucosal AngⅡ levels, inhibited the decrease of GMBF and decreased ulcer index and gastric mucosal damage (P<0.001, <0.01, <0.01, <0.01 and <0.05, respectively). Conclusion The endogenous AngⅡ plays a significant pathogenetic role in the development of stress ulcer in obstructive jaundice rats, and ACEI may prevent stress ulcer.
