Remote postconditioning by brief renal ischemia and reperfusion reduces acute myocardial ischemia and reperfusion induced myocardial apoptosis in rabbits.
- Author:
Song LIU
1
;
Xiang-feng WU
;
Wen-zhong ZHANG
;
Ying-xian SUN
;
Shang-lang CAI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Female; Ischemia; metabolism; Ischemic Preconditioning; Kidney Diseases; metabolism; Male; Myocardial Reperfusion Injury; metabolism; Myocardium; metabolism; Proto-Oncogene Proteins c-bcl-2; metabolism; Rabbits; bcl-2-Associated X Protein; metabolism
- From: Chinese Journal of Cardiology 2007;35(8):757-760
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVESTo observe the effects of renal ischemic postconditioning (RI-Post) on myocardial apoptosis in rabbits with acute myocardial ischemia and reperfusion.
METHODSAll rabbits were subjected to 60 minutes ischemia by left anterior descending coronary artery occlusion (LADO) and 6 hours reperfusion. The rabbits are randomly divided into 3 groups (n = 8 in each group): (1) Ischemia-reperfusion (IR): LADO and reperfusion without additional intervention; (2) RI-Post: after 60 minutes of LADO, the left renal artery was occluded for 30 seconds and reperfused for 30 seconds and repeated 3 times, then the coronary artery was reperfused for 6 hours; (3) Medication intervention (MI): 10 minutes before coronary reperfusion, rabbits were treated with PKC antagonist GF109203X (0.05 mg/kg, IV), followed by RI-Post treatment and 6 hours coronary reperfusion. Myocardial apoptosis was measured by TUNEL and the myocardial Bcl-2 and Bax protein expressions were assessed by immunohistochemistry.
RESULTSCompared with the IR group and the MI group, myocardial apoptosis was significantly reduced (P < 0.05) and the Bcl-2 protein expression increased (P < 0.01) while the Bax protein expression decreased (P < 0.05) in the RI-Post group.
CONCLUSIONSRemote renal postconditioning applied right before the onset of coronary artery reperfusion can reduce the myocardial apoptosis induced by myocardial ischemia and reperfusion and up-regulate Bcl-2 while down-regulate Bax expression possibly by activation of protein kinase C.