关键词：消化性溃疡；内皮缩血管肽-1；胃粘膜
摘 要 采用SD大鼠冷束缚应激溃疡模型(CRS)，动态检测了应激前及应激后1、3、6、9、12 h各时相血浆、胃粘膜组织内皮素-1(ET-1)含量、胃粘膜血流量(GMBF)及溃疡指数(UI)的变化，并观察内皮素转化酶抑制剂Phosphoramidon对应激性溃疡(SU)时GMBF、UI的影响。结果显示：应激后血浆、胃粘膜组织ET-1含量均较正常对照明显升高(P<0.05)，其中血浆ET-1于6 h达峰值后虽有所下降，但12 h以内仍高于正常；而胃粘膜组织ET-1则持续显著上升并与UI呈显著正相关(r＝0.974，P<0.01)，与GMBF呈显著负相关(r＝-0.842，P<0.01)，应用Phosphoramidon的应激组GMBF明显回升、UI明显下降(P<0.01)。提示内源性ET-1参与了CRS大鼠SU的发病过程，其机制是通过减少GMBF而引起胃粘膜缺血、糜烂与溃疡。而Phosphoramidon对SU具有一定的防治作用。
中国图书资料分类号 R573.1
ROLE OF ENDOTHELIN-1 IN COLD-RESTRAINT-STRESS-INDUCED ULCERS IN RATS
Li Zhaoshen, Duan Yiming, Zhan Xianbao et al.
Changhai Hospital, The Second Military Medical University, Shanghai 200433
Abstract The cold-restraint-stress-induced ulcer model in rats was used to observe the change of endothelin(ET)-1 levels in plasma and gastric mucosa, gastric mucosal blood flow(GMBF) and ulcer index(UI) prior to stress and 1、3、6、9 and 12 hours poststress. and the effects of phosphoramidon, an endothelin-converting-enzyme inhibitor(ECEI), on the GMBF and UI in rats with stress ulcer. The results showed that both plasma and gastric mucosal ET-1 levels increased significantly after stress compared with the controls (P<0.05), and plasma ET-1 showed a peak at 6 hours poststress, and then remained markedly higher than controls within 12 hours, while gastric mucosal ET-1 levels continued to increase significantly after stress. There was a positive relationship between gastric mucosal ET-1 and UI (r=0.974 ......
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