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目的 :观察肢体缺血再灌注 (LIR)对胃粘膜的损伤 ,探讨肢体缺血再灌注对胃粘膜损伤的作用及其部分机制 ,以及短暂多次肢体缺血在胃粘膜损伤发生中的作用。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后以及应用缺血预适应干预对胃粘膜损伤的影响 :取各组胃粘膜制作切片于光学显微镜和电子显微镜下进行观察 ,测定各组胃粘膜损伤指数、胃粘膜血流量 (GMBF)、胃结合粘液量、胃粘液中磷脂、氨基己糖的含量、血浆和胃组织一氧化氮含量以及胃粘膜一氧化氮合酶 (NOS)活性。结果 :光学显微镜和电子显微镜观察结果显示大鼠LIR后胃粘膜损伤严重 ,IPC组各类细胞损伤较LIR组轻 ;LIR后GMBF及胃结合粘液量、胃粘液中磷脂、氨基己糖的含量均低于对照组 ,虽然IPC组大部分指标与对照组有差异 ,但与LIR组对比GMBF及胃结合粘液量、胃粘液中磷脂、氨基己糖的含量均较高于LIR组 ;LIR组血浆与胃粘膜组织NO含量及NOS活性显著高于对照组 ,而IPC组血浆与胃粘膜组织NO含量和胃粘膜的NOS活性又显著高于LIR组。结论 :肢体缺血再灌注可导致胃粘膜损伤 ;缺血预适应可减轻肢体缺血再灌注后的胃粘膜损伤
OBJECTIVE: To observe the injury of gastric mucosa caused by limb ischemia-reperfusion (LIR), investigate the effect of limb ischemia-reperfusion on gastric mucosal injury and its mechanism, and the role of transient limb ischemia in the development of gastric mucosal injury. Methods: The rat LIR model was reproduced by Rosenthal method. The effects of ischemic preconditioning on gastric mucosal injury were observed and measured 4 h after ischemia and 4 h reperfusion. The sections of gastric mucosa of each group were made by light microscope and electron microscope The gastric mucosal lesion index, gastric mucosal blood flow (GMBF), gastric mucus volume, phospholipid and hexosamine contents in gastric mucosa, nitric oxide content in plasma and gastric mucosa, and nitric oxide content in gastric mucosa Enzyme (NOS) activity. Results: The results of optical microscope and electron microscope showed that the damage of gastric mucosa in LIR rats was severe, and the damage of various cell types in IPC group was lighter than that in LIR group. The contents of GMBF and gastric mucus, gastric phospholipid and hexosaminoglycan Compared with the control group, although most of the indicators in the IPC group were different from those in the control group, the levels of GMBF and gastric mucus in the LIR group were significantly higher than those in the LIR group The content of NO and the activity of NOS in gastric mucosa were significantly higher than those in control group, while the NO content in plasma and gastric mucosa and the activity of gastric mucosal NOS in IPC group were significantly higher than those in LIR group. Conclusion: Limb ischemia-reperfusion can lead to gastric mucosal injury. Ischemic preconditioning can reduce gastric mucosal injury after limb ischemia-reperfusion