| Objective Mechanism of myocardial protection of new inhalation anesthetic sevoflurane shortage is a bottleneck to the widely clinical use. It can effectively reduce myocardial ischemia and hypoxia injury is to reduce the operation complications of heart, It is an important way to improve the survival rate. In recent years, many studies have found that sevoflurane preconditioning on myocardial ischemia reperfusion has an important protection role, and lead to myocardial ischemia and hypoxia in the myocardium superoxide overproduction is an important source of myocardial injury. This study was to investigate the effects of sevoflurane on cyclooxygenase (COX-2) which is source of superoxide anion in myocardial ischemia reperfusion injury.Methods6-8weeks normal adult mice were randomly divided into three groups: control group (sham group), ischemia-reperfusion group(I/R group) and sevoflurane preconditioning group (SP group). The use of no artificial respiration rapid ligation of the left coronary artery method to establish the mouse myocardial ischemia-reperfusion model, Sham pseudo-operation group, I/R group ligation the LCA30min, loose the tie in vitro; SP groups2.0%sevoflurane pretreatment three times (15min/time) interval (15min/times) processing, then establish the I/R model. COX-2was measured at6h of reperfusion, Caspase3was determined at9h of reperfusion, left ventricular diastolic pressure (LVDEP) were recorded at24h of reperfusion.Results The results of animal experiments:Compared with Sham group, I/R group LVEDP increased (p<0.01), compared with I/R group, SP group LVEDP decreased,(p<0.01). Compared with Sham group, the level of Caspase-3increased in I/R group.(2.2±0.5vs9.1±0.5, p<0.01) compared with I/R group, Caspase-3decreased level of SP group,(9.1±0.5vs6.2±0.5, P<0.01), statistically significant difference between SP group and I/R group Caspase-3. Compared with Sham group, I/R group, Cox-2expression level increased; compared with I/R group, decrease the level of Cox-2in group SPConclusion Sevoflurane preconditioning significantly improve myocardial ischemia-reperfusion injury in mice, and the mechanism of the protective effect could be related to inhibit COX-2expression, play against myocardial nuclear apoptosis. |