一氧化氮及其合酶在心肌缺血再灌注损伤中作用的研究

目的：用鼠的离体工作心脏研究心肌缺血再灌注损伤一氧化氮（ＮＯ）、ＮＯ合酶（ＮＯＳ）的作用。方法：ＲＴ－ＰＣＲ定量检测心肌组织结构型ＮＯＳ（ｃＮＯＳ）的ｍＲＮＡ表达，测定心肌组织的ｃＮＯＳ、诱导型ＮＯＳ（ｉＮＯＳ）及冠状动脉动脉冠脉）流出液的ＮＯ，同时检测心脏缺血再灌注前后的心功能变化。并分别于次序停跳液中加用缓激肽（ＢＫ）、Ｌ－精氨酸及ＢＫ加Ｌ－精氨酸，观察其对心肌缺血再灌注损伤的影响。结果：心肌

The effect of nitric oxide and its synthase on myocardial ischemic reperfusion injury

Aim:The study was focused on the effect of nitric oxide(NO) and NO synthase (NOS) on the isolated working rat heart after ischemic reperfusion injury.Methods:The gene expression of constitutive NOS (cNOS) was quatified by reverse trancription-polymerase chain reaction (RT-PCR).The myocardial NOS content,the NO in effluent samples from coronary sinus was measured and the cardiofunction was assessed before and after ischemic reperfusion.The effects of Bradykinin(BK),L-argininne and BK L-arginine on myocardial ischemic reperfusion injury was evaluated.Results:The study demonstrated that the expression of cNOS mRNA was downregulated and NO,cNOS were reduced,but inducible NOS(iNOS) increased during ischemic reperfusion injury.In BK-treated group, compared with the control group of ischemic reperfusion,NO and NOS were increased,the recovery of myocardial function was improved. Compared with the control group,NO was increased in L-arginine-treated group,but the recovery rate of myocardial function was decreased .In BK L-arginine-treated group,compared with BK-treated group,NO was increased and the recovery of myocardial function was improved significantly.Conclusion:These results indicated that down-regulation of expression of cNOS mRNA and the change of isozymes of NOS could be one of the important mechanisms for the myocardial ischemic reperfusion injury.NO is double- edged but increasing cNOS may have effect of myocardial protection.