Effect Of Nitrates Postconditioning On The Myocardial Ischemia-Reperfusion Injury In Rat

Objective: In previous studies, ischemic postconditioning alleviated myocardial ischemia-reperfusion injury( MIRI) and protected myocardium, while its clinical applications is limited by the invasion. Therefore, the studies have paid more attention for pharmacological postconditioning. Recent studies showed that nitric oxide(NO) play an important role in the development of MIRI. The decreament of both endogenous and exogenous NO can attenuate MIRI. In the present study, we investigate the effects and mechanisms of nitrates postconditioning on the MIRI model of rat, and investigate whether the endoplasmic reticulun stress(ERS) can influence MIRI.Methods: Wistar rats were randomized into four groups(n=8) : sham operation group, ischemia-reperfusion group(I/R group), ischemia postconditioning group(IPost C group)and pharmacological postconditioning group(PPost C group). Relative markers are measured respectively in every group. Ischemic size and infarct size of myocardium are detected by both of Evan’s blue and TTC coloured. Serum c TNI are measured by ELISA. Cardiomyocyte apoptosis were determined by TUNEL. Grp78 and Caspase12 gene expression were detected by Fluorescence quantitative RT-PCR. Grp78 and Caspase12 protein expression were detected by Western-blot.Results:1. Compared with I/R group, IPost C and PPost C group significantly decreased the myocardial ischemic area, myocardial infarct size, c Tn I level and cardiomyocyte apoptosis(P<0.01). Compared with IPost C group, PPost C significantly decreased the myocardial ischemic area(P<0.05), while there was no significant difference of the myocardial infarct size, c Tn I level and cardiomyocyte apoptosis(P>0.05). 2.Compared with I/R group, Grp78 gene expression and protein expression in IPost C and PPost C group significantly increased(P<0.05), but but there was no significant difference between IPost C and PPost C group(P>0.05). Compare with I/R group, the Caspase12 gene expression and protein expression in IPost C and PPost C group significantly decreased(P<0.05), but there was no significant difference between IPost C and PPost C group(P>0.05).Conclusion: Nitrates PPost C, as well as IPost C, can reduce the myocardial ischemia-reperfusion injury via decreasing the myocardial ischemic area,myocardial infarct size, c Tn I level and cardiomyocyte apoptosis. Both ischemic postconditioning and nitrate pharmacological postconditioning can decrease cardiomyocyte apoptosis via lower the regulation ERS.