【摘要】 目的 :探讨蛋白激酶C(PKC)在兔肺缺血预处理保护中的作用。方法 :采用在体兔单肺原位缺血再灌注模型。 5 0只日本大耳兔随机均分为 5组。假手术组 (S)、缺血 /再灌注组 (I/R)、缺血预处理组 (IPC)、多粘菌素B组 (PMB)和缺血预处理加多粘菌素B组 (IPC +PMB)。实验末测血浆SOD活力和MDA含量 ,肺湿干重比和肺泡损伤数比值 ,观察肺超微结构变化。结果 :①I/R组与假手术组相比 ,SOD活力下降 ,MDA含量、湿干重比及肺泡损伤数比值增加 (P均 <0 .0 1)。IPC组与I/R组相比 ,SOD活力增加 ,MDA含量、湿干重比及肺泡损伤数比值下降 (P均 <0 .0 1)。I/R组、PMB组及IPC +PMB组之间的检测指标对比无明显变化 (P均 >0 .0 5 )。②电镜显示I/R组、PMB组及IPC +PMB组均有明显的肺超微结构损伤 ,而IPC组损伤不明显。结论 :缺血预处理对肺缺血再灌注损伤有明显的保护作用 ,且可被PKC抑制剂多粘菌素B取消 ,提示PKC参与肺缺血预处理的保护作用更多还原

【Abstract】 Objective:To investigate the effect of protein kinase C (PKC) on protection afforded by lung ischemic preconditioning in rabbits.Methods:Single lung in situ ischemic reperfusion animal model was used. 50 rabbits were randomly divided into five groups: sham group (S), ischemic reperfusion group(I/R), schemic preconditioning group(IPC), polymyxin B group(PMB)and ischemic preconditioning plus polymyxin B group(IPC+PMB). Wet to dry weight rate(W/D), injured alveoli rate, Superoxide dismutase (SOD) activity and maondialdehyde(MDA) content in plasma were examined, ultramicroscopic structure changes were observed at the end of experiment.Results:①the SOD activity of I/R group decreased and MDA content,W/D and injured alveoli rate increased compared with S group(P<0.01.respectively). Higher SOD activity, lower MDA content ,W/D and injured alveoli rate were found in IPC group than that in I/R group(P<0.01). There were no significant change of above assessed indexes in IPC +PMB group compared with I/R group(P>0.05). ②Electron microscope showed serious pulmonal ultramicroscopic structure injury was occurred in I/R group, PMB group and IPC+PMB group, but no significant injury was found in IPC group.Conclusion:Ischemic preconditioning protect lung against ischemia /reperfusion injury and its protective effect can be blocked by Polymyxin B,it suggests protein kinase C participate the protection afforded by lung ischemic preconditioning.更多还原