Objective To investigate the effects and mechanism of the pretreatment with simvastatin on the area of myocardial infarction in reperfusion injury rabbits after acute myocardial infarction (AMI).
Method 20 New Zealand white rabbits were randomly divided into four groups: group A, AMI/reperfusion; group B, pretreated with simvastatin (5 mg/kg) for 3 days before AM I; group C, treated with glibenclamide (KATP channel blocker) (5 mg/kg) before AMI, group D, treated with glibenclamide and simvastatin before AMI. Models of AMI/reperfusion were established by 180-min of coronary occlusion and 60-min of reperfusion. At the end of reperfusion, the coronary artery was reoccluded, and the risk zone was delineated with Evan’ blue. Hearts were sectioned (2 mm) and incubated in 1% TTC in phosphate buffer for 20 min to define white necrotic tissue when fixed in 10% formalin for 24 h, and the level of plasma creatine kinase-MB was assessed and evaluated.
Result (1)The content of CK-MB was significantly decreased in group B than that in group A and group C (P<0.01), however, it was markedly decreased in group D than those of group A, and significantly increased than that of group B. (2) The risk zone volumes were similar among all the groups. The infarct size was (43.6±4.6)% in group A, Simvastatin treatment resulted in a significant limitation of infarct size in group B (23.6±2.8% VS group A, P<0.01), the infarct size was similar in group C (45.1±4.5%) compared with that in group A (P>0.05). However, it was markedly decreased in group D (36.8±3.4%) than that of group A (P<0.05), and significantly increased than that of group B (P<0.05).
Conclusion Simvastatin significantly reduced myocardial infarct size and the level of plasma myocardial enzyme during AMI and reperfusion in rabbits, which has protective effects on ischaemic/reperfused myocardium, and the activation of ATP-sensitive K channels might be involved in this protective mechanism.