摘要
目的观察肠缺血预处理(IPC)对缺血再灌注(I/R)损伤的保护作用,探讨IPC在肠I/R损伤中的作用机制。方法对大鼠肠系膜上动脉进行4次循环的5min夹闭/5min开放(即IPC),24h后实施缺血30min再灌注24h,制作I/R损伤模型。检测IPC后肠组织一氧化氮(NO)含量(以NO2-/NO3-代表)、超氧化物歧化酶(SOD)、丙二醛(MDA)的含量及观察肠肌间神经丛一氧化氮合成酶(NOS)阳性神经元的变化,检测血清NO及血浆二氨氧化酶(DAO),采用Chiu评分法观察肠组织损伤情况。结果IPC后肠组织NO、SOD含量下降,而MDA含量明显升高,肠肌间丛NOS阳性神经元数明显降低,DAO水平明显降低,肠组织损伤程度明显减轻。结论IPC对I/R损伤有明显保护作用,其机理与灭活了氧自由基,降低NO含量有关。
Objective： To investigate the machanism of the protective effects of intestinal preconditioning （IPC）on ischemie reperfusion（I/R）injury. Method： Rats were preconditioned with 4 cycles for 5 min superior mesenterie artery occlusion/5min reperfusion and 24 h later perforned 30 min superior mesenteric artery occlusion followed by 24 h reperfusion. The changes of malonaldehyde （MDA）, superoxide dismutase（SOD）, nitric oxide （NO）and nitric oxide synthase（NOS）positive neurons in the intestinal tissue were observed after IPC. Chiu＇s count was used to assess the changes in intestinal pathological morphology. Serum NO and hematoplasma DAO Were also examined 24 h after IPC. Results IPC significantly decreased the levels of NO. MDA and increased the activity of SOD and decreased the number of NOS positive neurons. Conclusion：IPC protects intestine from I/R injury. The mechanism may be inactivation of the oxygen free radicals and decreasing NO.
出处
《山东医药》
CAS
北大核心
2006年第9期13-14,共2页
Shandong Medical Journal
基金
温州市科技计划项目(Y2004A143)
关键词
缺血预处理
再灌注损伤
自由基
活性氧
肠缺血
ischemic preconditioning
reperfusion injury
intestinet free radical
active oxgen
