异丙酚对大鼠小肠缺血再灌注后肺损伤磷脂酶A_2变化的影响

Effects of propofol on the changes of PLA_2 in rat lung after intestinal ischemia reperfusion

目的 :探讨临床剂量异丙酚对大鼠小肠缺血再灌注后肺损伤磷脂酶A2 (PLA2 )变化的影响及其保护作用。方法 :雄性SD大鼠 12 0只 ,随机分为假手术对照组 (Ⅰ组 )、小肠缺血再灌注组 (Ⅱ组 )及给予异丙酚每小时 10mg/kg(Ⅲ组 ) ,制作小肠缺血再灌注模型。以12 5I标记白蛋白肺摄取指数作为肺损伤的指标 ,以髓过氧化物酶活性作为评价多形核中性粒细胞 (PMN)在肺组织聚集的指标 ;实验结束即刻留取肺组织 ,待测肺组织形态学变化。结果 :异丙酚可明显抑制小肠缺血再灌注后肺组织髓过氧化酶 (MPO)、PLA2 活性升高 (P <0 .0 1) ,降低12 5I标记白蛋白肺摄取指数 (P <0 .0 1) ;Ⅰ组肺组织结构正常 ,Ⅱ组可见肺泡压闭实变 ,腔内有大量渗出 ,炎性细胞浸润 ,毛细血管扩张 ,支气管壁增厚 ,腔内有渗出 ,出血 ;Ⅲ组肺部改变较Ⅱ组明显减轻 ,除了有少量渗出、肺泡壁稍为增厚、毛细血管轻微扩张外 ,肺组织结构基本接近正常。结论 :PLA2 在大鼠小肠缺血再灌注后肺损伤中有重要作用 ,临床剂量异丙酚可明显降低肺组织内PLA2 活性增高 ,改善肺毛细血管通透性改变 ,产生肺保护作用。

Objective: To study the effects of propofol on the changes of PLA 2 in rat lung after lung injury induced by intestinal ischemia reperfusion (IIR). Methods: Male Sprague Dawley rats (120) weighing 200 to 250 mg were randomly divided into group Ⅰ(sham operation ), group II (super mesenteric artery occlusion for 60 minutes and reperfusion for 120 minutes) , group Ⅲ (super mesenteric artery occlusion with propofol 10 mg/kg per hour). Lung uptake of 125 I-labeled albumin and myeloperoxidase were assayed as indexes of pulmonary microvascular leak and accumulation of polymorphonuclear neutrophils in lung respectively. The concentration of phospholipase-activiting factor A 2 in lung tissue were observed. Morphologic changes of lung were examined. Results: Propofol could oberviously inhibit the increase of activity of myeloperoxidase (MPO) in lung and 125 I-labeled albumin uptake index, and decreased the concentration of PLA 2 in lung(P<0.01). The histological examination of lung revealed negligible alterations in the group Ⅰ and Ⅲ, whereas in the group II a significant increase of infiltration in interstitial space and substantial thickening of the alveolar septa showed. Conclusion: The PLA 2 plays an important role in the lung injury induced by intestinal ischemia-reperfusion, and the propofol of clinical dose has protective effects on the lung injury by inhibiting the activity of MPO and PLA 2 in lung and ameliorating the pulmonary microvascular penetrability.