【摘要】 目的 :探讨缺血预适应 (IP)对在体肺脏细胞间粘附分子 - 1(ICAM- 1)表达的影响。方法 :SD大鼠 36只 ,随机分为 3组 :假手术 (SO)组 ;缺血再灌注 (I/R)组 ;IP组。左侧开胸 ,建立肺脏 I/R模型。应用 IP,以免疫组化方法观察肺脏 ICAM- 1表达 ,测定肺髓过氧化物酶 (MPO)及超氧化物歧化酶 (SOD)活性 ,以及肺湿重 /干重比值 (W/D)。结果 :IP后肺脏 ICAM- 1表达显著降低 ,MPO活性显著降低 ,SOD活性增高。结论 :IP可抑制 I/R后肺脏 ICAM- 1的表达 ,从而减少局部白细胞浸润 ,减轻肺脏结构损害 ,减轻肺水肿。更多还原

【Abstract】 Objective:To investigate the effect of ischemic preconditioning on the expression of ICAM-1 in lung in vivo after lung ischemia-reperfusion in rats.Methods:Thirty-six male Sprague-Dawley rats were randomized to three groups (twelve control, twelve ischemia-reperfusion, twelve ischemic preconditioning). I/R injury consisted of 45 minutes of lung cross-clamping followed by 5 hours of reperfusion; ischemic preconditioning applied 3 periods of 5 minutes of ischemia and/5 minutes of reperfusion immediately preceding I/R; control animals had a thoracotomy only. Lung tissue wet-to-dry weight ratio and myeloperoxidase concentration were markers of edema and neutrophil sequestration respectively. Superoxide dismutase activity were assessed, also. Expression of ICAM-1 in lung was measured immunohistochemically to observe the changing of lung tissue in pathology under Electron Microscopy and Light Microscopy.Results:Expression of ICAM-1 decreased significantly after ischemic preconditioning, the myeloproxidase activity decreased too, and superoxide dismutase activity increased.Conclusion:Ischemic preconditioning could inhibit the expression of ICAM-1 after ischemia-reperfusion injury, and reduce neutrophil-infiltration in lung, and attenuate ultrastructure injury of lung tissue, then attenuate pulmonary edema.更多还原