Objective: To test the hypothesis that limb ischemic postconditioning protects the myocardium from reperfusion injury, and examine the mechanism involved.
Design: Forty rabbits were randomly divided into four groups: Control, Ischemic Preconditioning, Ischemic Postconditioning and Remote Postconditioning. Myocardial infarct size and tissue myeloperoxidase activity were determined at the end of the experiment. Plasma creatine kinase and malondialdehyde activity were measured at baseline, the end of ischemia, and after 3 h of reperfusion respectively.
Results: Myocardial infarct size was significantly reduced in Ischemic Preconditioning, Ischemic Postconditioning and Remote Postconditioning as compared to Control (p < 0.01). Results were confirmed by plasma creatine kinase activity. Plasma malondialdehyde was significantly less at 3 h of reperfusion in Ischemic Preconditioning, Ischemic Postconditioning and Remote Postconditioning than that in Control (p < 0.01). Neutrophil accumulation (myeloperoxidase activity) in the area at risk was less in Ischemic Preconditioning, Ischemic Postconditioning and Remote Postconditioning than that in Control (p < 0.01).
Conclusion: Remote postconditioning reduces myocardial infarction in rabbits. The mechanism involved might be reduced oxygen radical-induced injury and improved antioxidant action.