The Effect of Postconditionoing on Inflammatory Response Induced by Myocardial Ischemia-Reperfusion Injury in Rat

Ischemic heart diseases are the leading cause of mortality in modern society and postconditioning is considered as a new therapeutic strategy in cardioprotection against ischemic insults. The purpose of this study was to investigate the effect of ischemic postconditioning on inflammation caused by ischemia-reperfusion myocardium injury in rat.

In this experimental study, 21 male Wistar rats were used and divided into three groups: control, ischemia-reperfusion and postconditioning. After surgery, the hearts of rats were isolated and mounted on a Langendorff apparatus with a constant pressure. In second and third groups, after 15-minutes stabilization period of cardiac function‚ the hearts were exposed to 30-minutes regional ischemia by occlusion of left anterior descending coronary artery and followed by 60-minutes reperfusion. In third group (postconditioning), postconditioning was exerted at the start of reperfusion by applying 3 alternative cycles of 30 seconds reperfusion and ischemia. The resulting supernatants of samples from ischemic zone of left ventricle were used to measure creatine kinase (CK) enzyme as in indicator of damage and inflammatory factors interlukin-6 (IL-6) and tumor necrosis factor (TNF-α) using laboratory kits via ELISA assay.

Ischemia-reperfusion significantly increased the level of myocardial CK enzyme as compared with control group (27±3 vs. 12±4 U/l) (p<0.05). In addition, the levels of inflammatory agents IL-6 and TNF-α were significantly increased in I/R group (p<0.05). Induction of postconditioning significantly reduced the CK level to about 17±3 U/l in third group and significantly decreased the levels of IL-6 and TNF-α as compared with those of I/R group (p<0.05).

Postconditioning can protect the heart by preventing the production of inflammatory agents in myocardium, and thereby reduce the reperfusion injury.