门奇静脉断流术致胃壁缺血的研究  

Experimental study on gastric mocusa ischemia after cardio-gastric devascularization

作　　者：姚常柏[1] 夏振龙[1] 张丽红[1] 

机构地区：[1]中国医科大学第二临床学院普外科

出　　处：《肝胆外科杂志》1994年第1期4-8,共5页Journal of Hepatobiliary Surgery

基　　金：国家自然科学基金

摘　　要：缩窄家兔门静脉主干制成门静脉高压模型，从组织学、胃壁微循环血液灌注量、胃粘膜前列腺素Ｅ２含量的变化等３个方面探讨了门奇静脉断流术对门脉高压家兔胃壁缺血性改变的影响及其机制。结果表明：①门静脉高压时胃粘膜的损害是与粘膜下层瘀血、粘膜防御屏障受损、粘膜前列腺素Ｅ２含量的降低有关。②门奇静脉间反常血流阻断愈彻底，胃粘膜缺血性损害愈严重。③联合断流术较贲门周围血管离断术致胃粘膜损害更加严重的原因可能是由于联合断流术时行胃底横断后进一步加剧了胃粘膜下层血流灌注量的不足．粘膜层细胞缺血、缺氧及前列腺素Ｅ２含量降低的结果。Portal hypertension of rabbit was produced by constricting main portal vein.Mechnism and effect of the gastric mucosa ischemia were studied after pericardial devascularization or with gastric bottom transection by histologic, gastric microcirculation infusion, gastric mucosa prostaglandin E2. The results showed that: (1 ) Gastric mucosa lesion of the portal hypertension rabbit was consistent with ischemia and congestive mucosa barn e damage due to decrease of prostaglandin E2. (2) The more abnormal blood flow between protal vein and azygosvein were blocked, the more gastric mucosa was damaged. (3 ) Gastric mucosa lesion of devascularization with gastric bottom transection Was more serious than only devascularization because insuffucient of the gastric microcirculation infusion and lesion of gastric mucosa barrier and decrease of gastric mucosa prostaglandinE2 became more serious after gastric bottom transection.

关 键 词：门脉高血压 门奇静脉 断流术 缺血 

分 类 号：R657.340.5[医药卫生—外科学]