环氧合酶2介导地氟醚延迟预处理对大鼠心脏的保护作用

Cardioprotective effect of delayed preconditioning with desflurane mediated by cyclooxygenase-2 in rats

目的:探讨环氧合酶2介导地氟醚延迟预处理对大鼠心脏的保护作用。方法:32只Wistar大鼠随机分为对照组、NS398组、地氟醚延迟预处理组(DES)及NS398+DES组,建立心肌缺血/再灌注模型,以TTC染色法测定梗死心肌大小;另取32只Wistar大鼠,分组同上,RT-PCR测定缺血区心肌COX-2mRNA水平。结果::地氟醚延迟预处理(1MAC)可显著减少大鼠缺血/再灌注后心肌梗死的范围(P<0.01),并可使心肌COX-2mRNA表达增强(P<0.01),其心脏保护作用可被COX-2选择性抑制剂NS398阻断。结论:环氧合酶2介导地氟醚延迟预处理对大鼠心脏具有保护作用。

Objective： To investigate whether the cardioprotective effect of delayed preconditioning with desflurane in rats is mediated by cyclooxygenase-2（ COX-2）. Methods： The rat model of myocardial ischemia/reperfusion （I/R） was established by occlusion of left anterior descending artery for 30 minutes and reperfusion for 2 hours. A total of 32 Wistar rats were randomly divided into 4 groups ： control group, NS-398 group （ the selective COX -2 inhibitor, NS398 of 5 mg/kg, was injected intraperitoneally 24 hours before I/R） , DES group （ rats were preconditioned with 1 MAC of desflurane 24 hours before I/R） , and NS398 ＋ DES group （ NS398 of 5mg/kg was injected intraperitoneally 30 minutes before preconditioning with 1 MAC of desflurane and I/R was established 24 hours later）. After reperfusion, the hearts were sampled and stained with TTC, and the infarct size was measured. Another 32 Wistar rats were grouped and treated the same way as above mentioned. Reverse transcription polymerase chain reaction was performed to measure the level of COX-2 mRNA in infracted myocardium. Results： Delayed preconditioning with 1 MAC desflurane significantly decreased the infarct size after I/R and significantly increased the level of COX -2 mRNA in infracted myocardium, and such effects of delayed preconditioning with desflurane were inhibited by NS-398. Conclusion： Cardioprotective effect of delayed preconditioning with desflurane is mediated by COX-2 in rats.