The Study Of The Protection And Mechanism Of Renal Ischemic Postconditioning On Myocardium With Acute Myocardial Ischemia And Reperfusion Injury

Objectives: In this study, we tested the hypothesis that renal ischemicpostconditioning(RI-Post) protects the rabbits myocardium from acute myocardialischemia and reperfusion injury, and compared this strategy with myocardial ischemicpostconditioning, then examined the mechanism involved.Methods: All rabbits were subjected to a total of 60 minutes of left coronary arteryocclusion (LCAO) and 6 hours of reperfusion. The rabbits were randomly divided intofour groups(n=8 in each group): 1) Ischemia-reperfusion(IR): LCAO and reperfusion onlywith no other intervention;2)Ischemic preconditioning(IPC): Three cycles of myocardialischemia(5min) and reperfusion(10min) preceded the 60 minutes of left coronary arteryocclusion (LCAO) and 6 hours of reperfusion;3) Renal ischemicpostconditioning(RI-Post): after 60 minutes of LCAO the left renal artery was occluded30 seconds and released 30 seconds for three cycles, then the coronary artery was perfused6 hours;4)Medicine intervention(MI): after 50 minutes of LCAO rabbits were received0.05 mg/kgⅣof the PKC antagonist GF109203X, then the left renal artery was occluded30 seconds and released 30 seconds for three cycles at coronary artery reperfusion. Thehemodynamics were monitored at before ischemia. ischemia 5 min, ischemia 1h andreperfusion 3h and reperfusion 6h; The CK-MB and cTNI were measured three times:before LCAO, reperfusion 3h and reperfusion 6h; After the experiment, TUNEL wasapplied to monitor the myocardium apoptosis, Bcl-2 and Bax protein expression wereassessed by immunohistochemistry.Results: The changes of hemodynamics were less in the IPC and RI-Post than the IR(P＜0.05); Compared with the IR, The levels of CK-MB and cTNI were reducedsignificantly (p＜0.05) at reperfusion 3h and reperfusion 6h in the IPC andRI-Post; Compared with the IR, The levels of the myocardium apoptosis index werereduced significantly (p＜0.05), the Bcl-2 protein expression was increased (P＜0.05), onthe contrary, the Bax protein expression was induced (P＜0.05) in the IPC andRI-Post; GF109203X abolished the effects of Renal ischemic postconditioning. Conclusions: Remote renal postconditioning applied immediately before the onset ofcoronary artery reperfusion protects the ischemia myocardium, which is similar to thecardioprotective effect of myocardial ischemic preconditioning. This inter-organ remotepostconditioning phenomenon is likely mediated in part by activation of PKC by theischemic-reperfused kidney.