大鼠肢体缺血-再灌注所致胃粘膜损伤及其机制

目的：观察肢体缺血再灌注（LIR）对胃粘膜的损伤作用。探讨其可能的作用机制。方法：按Rosenthal方法复制大鼠LIR模型。观察并测定肢体缺血4h再灌注4h后胃粘膜的损伤性变化。测定各组胃粘膜损伤指数。检测胃粘膜中髓过氧化物酶（MPO），超氧化物歧化酶（SOD），丙二醛（MDA）及黄嘌呤氧化酶（XOD）含量的变化，以及血浆中MDA，XOD，SOD含量的变化。结果：大鼠LIR后胃粘膜损伤严重。胃粘膜损伤指数增加；胃粘膜中MPO-MDA，XOD的值均较对照组增加，血浆中MDA，XOD的值亦较对照组显著增加，血浆及胃粘膜中SOD的酶活力下降。结论：肢体缺血再灌注作为应激原可引起胃粘膜损伤，导致应激性溃疡的发生；自由基在肢体缺血再灌注后继发胃粘膜损伤过程中有一定作用。

The mechanism of the gastric mucosal injury following ischemia reperfusion of hind limbs of rats

Objective:To observe the degree of gastric mucosal injury following limb ischemia reperfusion(LIR),and to investigate the mechanism of gastric mucosal injury.Methods:Referring to Rosenthal's method, the model rats which underwent 4 hours of ischemia and 4 hours of reperfusion of hind limbs were made.Then to observe and determine the indexes of gastric mucosal injury after I/R respectively.The values of MPO,SOD,MDA and XOD in gastric mucosa and the values of MDA,XOD,and SOD in plasma were detected.Results: Serious damage in gastric mucosa was observed after LIR.After LIR, compared to the control group, the histologic lesion score were increased significantly; the value of MPO,MDA,XOD in gastric mucosa and the values of MDA,XOD in plasma were increased remarkably and SOD activity in gastric mucosa and in plasma were decreased.Conclusion:LIR can lead to the development of stress ulcer; oxygen free radicals plays an important role in it.