摘要
目的:观察大鼠肾脏缺血预处理(R IP)后心肌缺血再灌注(M IR)时细胞间粘附分子-1(ICAM-1)mRNA表达和一氧化氮(NO)水平的变化,探讨缺血预处理对心肌缺血再灌注损伤的影响。方法:大鼠35只,分为假手术对照(sham)组、M IR组、R IP+M IR组,后两组又分为缺血30m in、再灌注60m in、120m in等三个时相。取缺血心肌用原位杂交法检测ICAM-1mRNA表达水平,检测血清(NO)含量及一氧化氮合酶(NOS)活性,进行中性粒细胞(PMN)计数。结果:与Sham组比较,M IR组和R IP+M IR组再灌注各时相ICAM-1mRNA表达均显著增加。与M IR组再灌注对应时相比较,R IP+M IR组ICAM-1 mRNA表达均显著减少。M IR组缺血30m in时相与Sham组相比NO、NOS无差异,再灌注后NO、NOS开始下降,随时间延长,NO、NOS逐渐减少。与M IR组再灌注对应时相比较,R IP+M IR组NO及NOS均显著增加。缺血后再灌注时随时间延长,PMN数量逐渐增加,缺血预处理干预后PMN数量显著下降。结论:心肌缺血后再灌注时有大量PMN浸润,与心肌损伤关系密切。ICAM-1参与介导了中性粒细胞对内皮细胞的粘附、浸润和M IR的发生、发展,R IP通过减少ICAM-1 mRNA表达水平减轻M IR所致的心肌损伤。R IP通过增加NO,减少PMN浸润减轻随后的缺血再灌注损伤,起心肌保护作用。
Objective ：To observe the change of intercellular adhesion molecule expression and nitric oxide in ischemic-reperfused myocardium after renal ischemic preconditioning and to investigate the effect of ischemic preconditioning on myocardial ischemic-reperfusion injury. Methods ： hirty-five rats were divided into three groups： Sham-group, MIR and RIP ＋ MIR group. The last two groups underwent ischemia for 30 minutes, reperfusion for 60mim and 120min. The level of expression of ICAM-1 mRNA in myocardium was evaluated by method of in Situ Hybridization. The changes of serum nitric oxide and nitric oxide synthase were examined. The numbers of PMN were counted. Results： Comvared with sham group, the expression levels of ICAM-1 mRNA in MIR and RIP＋MIR groups was increased significantly. Compared with MIR groups, the expression levels of ICAM-1 mRNA was decreased significantly in RIP＋MIR groups. No difference was found between sham group and MIR group 30 minutes after ischemia. The levels of nitric oxide and nitric oxide synthase were decreased significantly after reperfusion. Compared with MIR groups, the levels of nitric oxide and nitric oxide synthase were increased significantly in RIP＋MIR group. The number of PMN was significantly increased in ischemic-reperfused myocardium. The numbers of PMN were significantly decreased in ischemic-reperfused myocardium after renal ischemic preconditioning. Conclusions： The findings indicate that PMN could induce myocardial ischemic reperfusion injure after MIR, which result from the ICAM-1 mediated PMN adhesion. The myocardial neutrophils infiltration indicates that neutrophils participate in impairing the myocardium during myocardial ischemic reperfusion. Ischemic preconditioning prevents the neutrophils from myocardial infiltration, and ameliorates the ischemic reperfusion injury by the increasing levels of the nitric oxide.
出处
《陕西医学杂志》
CAS
北大核心
2006年第12期1582-1585,共4页
Shaanxi Medical Journal
基金
江苏大学青年自然科学基金(JDQ03029)
