一氧化氮在大鼠胰腺缺血/再灌注中的变化及作用

目的:探讨一氧化氮(NO)在大鼠胰腺缺血/再灌注损伤中的变化及作用.方法:雄性Wistar大鼠随机分成3组:A、B组胰腺缺血30 min后,再灌注2,4,6,12,24h.B组再灌注前使用诱导型一氧化氮合酶(iNOS)抑制剂,A组仅给与生理盐水.C组仅行假手术.进行大鼠血清中NO水平和淀粉酶活性检测,胰腺组织形态学观察和免疫组化分析.结果:再灌注4 h后,A组iNOS表达于胰腺组织,B组无表达.此时A组NO水平达到高峰,淀粉酶活性开始升高,均高于B组(P＜0.01).再灌注6 h后,A组显微镜下观察到胰腺损伤的表现,B组未见.C组无iNOS表达,血清NO水平和淀粉酶活性均在正常范围.结论:随着再灌注时间的延长,iNOS表达于胰腺组织,NO在大鼠胰腺缺血/再灌注损伤中的有害作用占主导地位.

Effect of nitric oxide during ischemia/reperfusion injury in rat pancreas

Objective: To investigate the effect of nitric oxide(NO) during ischemia/reperfusion injury in rat pancreas.Methods:Male Wistar rats were randomly divided into 3 groups.The rat models of pancreatic ischemia were established in group A and B,and the rat models of sham-surgery were established in group C.The rats in group A and B were killed 0,2,4,6,12,and 24 hours after reperfusion.Before reperfusion,the rats received inducible nitric oxide synthase(iNOS) inhibitor in group B and received saline in group A.The NO level and amylase activity in the serum were measured,and the morphology of pancreas were evaluated under light microscope with HE staining and immunohistochemical staining.Results:Four hours after reperfusion,the expression of iNOS was seen in group A,but no expression was seen in group B.Meanwhile,the NO level reached the peak and the amylase activity increased obviously in group A,and both NO level and amylase activity in group A were higher than those in group B(P<0.01).Six hours after reperfusion,pancreatic injury was found under microscope in group A,but no injury was found in group B.In group C,there was no expression of iNOS,and the NO level and amylase activity in the serum were normal.Conclusion:With the prolongation of reperfusion,iNOS is expressed in pancreas tissues.The harmful effect of NO during ischemia/reperfusion injury is dominant.