摘要
目的了解特异性诱导型一氧化氮合成酶(iNOS)抑制剂氨基胍(AG)对大鼠肠缺血再灌注损伤的影响,进一步探讨一氧化氮(NO)与肠缺血再灌注损伤间的因果关系。方法制作大鼠肠缺血再灌注损伤的动物模型,其中部分大鼠应用AG进行干预,并于不同时点检测大鼠血浆NO含量、肠组织iNOS表达及肠道病理损伤情况。结果应用AG进行干预后,缺血阶段各项指标变化无显著性,而再灌注阶段血浆NO含量、肠组织iNOS表达及肠道病理损伤评分下降均有显著性。结论选择性iNOS抑制剂通过影响iNOS的合成及活性,减少了由NO介导的组织细胞损伤。进一步证实肠缺血再灌注过程中NO主要由iNOS合成,并发挥了重要的致损作用。
Objective To investigate the effect of aminoguanidin （AG）,a selective inhibitor of iNOS,on intestinal ischemia-reperfusion injury in rats ,and analyze the correlation of NO with intestine ischemia-reperfusion injury. Methods Thirty- six rats were divided into 6 groups consisting of A group with the ligation of arteriae mesenterica superior for 45 min, B group with same as A group and adding the reperfusion for 90 min, C group with same as A group and adding the reperfusion for 180 min,D group with same as A group and the administration of AG at a dose of 50mg/kg at 10 min before the ligation,E group with same as B group and the administration of AG at 10 min before both of the ligation and reperfusion,and F group with same as C group in intestinal ischemia time and E groups in AG administration,respectively. Plasmic NO content and the synthetic level of iNOS with immune histochemitry were measured,and intestinal pathological changes were scored with Chiu pathological grade under light microscope in all rats of 6 groups. Results There were no significant differences in plasmic NO content,synthetic level of iNOS and pathological changes before and after AG administration during the ischemia stage （P 〉 0.05 for all）. However,above parameters decreased significantly after AG administration during the reperfusion stage （P 〈 0.01 for all）. Conclusions NO which is mainly produced by iNOS during ischemia-reperfusion period plays an important role in causing intestinal ischemia-reperfusion injury. It is feasible that the administration of AG can alleviate the injury by decreasing NO production and its activity.
出处
《临床儿科杂志》
CAS
CSCD
北大核心
2006年第8期689-691,共3页
Journal of Clinical Pediatrics
