一氧化氮对大鼠在体心肌缺血预适应作用的研究

目的:实验以缺血预适应模型为基础,研究一氧化氮(NO)在心肌缺血预适应延迟相中的作用。方法:实验将Wistar大鼠随机分为5组:假手术组、仅行缺血预适应处理的对照组、于延迟相给药的S-甲基琉脲硫酸盐(SMT)组、硝普钠(SNP)组和SMT+SNP组。测算各组动物血清NO2-+NO3-含量及CK-MB定量,观察NO的释放对心肌损伤、梗死面积的影响。心肌细胞超微结构的变化。结果:限制内源性NO的释放可降低心肌损伤的程度,缩小心肌损伤、梗死面积。结论:在心肌缺血预适应延迟相过程中,内源性NO加重心肌损伤程度,而外源性NO可减轻心肌损伤程度。

Role of nitric oxide in ischemic preconditioning

Objective： This study was undertaken to identify the effect of nitric oxide during ischemic preconditioning. Method： Wistar rats were randomly divided into five groups： 1. sham operation group （Sham）, 2. control group induced by ischemic preconditioning, 3. SMT group （ animals were treated i.v. with SMT 5 mg/kg body weight 24 hours after IP）, 4.SNP group （animals were treated i.v. with SNP 5 μg/kg·min 24hours after IP）, 5. SMT ＋ SNP group （animals were treated i.v. with SMT 5 mg/kg body weight and SNP 5 μg/kg· rain 24 hours after IP）. Nitrite ＋ nitrate content and CK-MB were analyzed. The infarction size and the injured area in each group were measured. The changes of myocardial structure were observed with microscope. Result： Nitrite ＋ nitrate and CK-MB content of blood serum in SMT, SNP and SMT group was lower than control group （ P 〈 0.05）. Both SMT and SNP treatment reduced infarction size and the injured area （P 〈 0.05） when compared with IP. Conclusion： In the Late Phase of Myocardial Ischemic Preconditioning, nitric oxide generated by the enzyme inducible NO synthase （iNOs） proved to increase myocardial injury, while nitric oxide produced by NO donor drug was effective at reducing the injury.