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Objective: To observe whether there are some differences between myocardial postconditioning and remote postconditioning, and whether there is additional cardiac protection when they are used combined during myocardial ischemia/reperfusion injury in rabbits., Methods: Thirty healthy New Zealand rabbits which were randomly divided into 5 groups (n = 5): ischemic control group (CON), sham operation group (Sham), myocardial postconditioning group (MPostC), remote postconditioning group (RPostC), myocardial postconditioning plus remote postconditioning group (MPostC + RPostC). Acute myocardial infarction was induced by 45 minutes occlusion on left circumflex coronary artery (LCX) and 2 hours reperfusion in all anesthetized open-chest rabbits except the Sham, the coronary occlusion and reperfusion were determined by changes of ECG and cardiac color. Skeletal muscle ischemia model was induced by extrinsic iliac arteries occlusion and reperfusion with artery clamps. The condition that the extrinsic iliac arteries were occluded or reperfused could be tested by according to the distal arterial pulse. Plasma creatine kinase (CPK) activity and lactate dehydrogenase (LDH) activity were measured at baseline, the end of ischemia, after 1 hour and 2 hours of reperfusion respectively. The extent of myocardial infarction was assessed by triphenyltetrazolium (TTC) staining and measured by area ratio of AN/AAR., Results: Compared with the Con, myocardial infarct size was significantly reduced in MPostC and RpostC group (P < 0.05). But there was no significant difference between MPostC and RPostC group. Combined MPostC and RPostC markedly enhanced myocardial protection (P < 0.05). The trend of CPK and LDH release was similar to the trend of myocardial infarct size., Conclusion: Both MPostC and RPostC induced cardiac protection. There was no significant difference between MPostC and RPostC. Combined MPostC and RPostC induced markedly additive effect on myocardial protection.

Objective: To investigate the effects of rabbit limbs ischemia/reperfusion on myocardial necrosis and apoptosis in vivo., Methods: Thirty-six healthy new zealand rabbits were randomly divided into 3 groups: (1) Sham group; (2) I/R(Ischemia/reperfusion) group; (3) RPostC (remote postconditioning) group. The activity of blood serum creatine kinase (CK) and lactate dehydrogenase (LDH) were measured at baseline, the end of ischemia after 60 min and 120 min of reperfusion respectively. The extent of myocardial ischemia and the scope of myocardial infarction were assessed by evans blue and Triphenyl tetrazolium chloride (TTC). The myocardial cell's apoptosis at the area of myocardial ischemia was estimated by Tunel. Protein expression of caspase-3, Bcl-2 and Bax in myocardial ischemic area were analyzed with the method of immunohistochemistry., Results: Compared with I/R group, the myocardial infarct size and the CK activity were significantly reduced in RPostC group. The Tunel positive index of RPostC group in ischemic myocardium was significantly lower than that in I/R group (21.79% +/- 1.07% vs 35.81% +/- 1.10%, P < 0.05). Caspase-3 positive cells index was calculated with randomly selected five regions in each slide and then the positive cells in per hundred cells were calculated. The RPostC group of caspase-3 positive cells was significantly lower than that in I/ R group(25.03% +/- 1.16% as 39% +/- 2.43%, P < 0.05). Compared with the sham group, the Bax protein expression index and the Bcl-2 protein expression index of I/R group and RPostC group were increased. The Bax/Bcl-2 ratio of RPostC group decreased, while it was increased in I/R. Compared with the I/R group, the Bax protein expression and Bax/Bcl-2 ratio of RPostC group significantly reduced, but the expression index of Bcl-2 ratio was significantly increased, the differences were statistically significant., Conclusion: Limbs ischemia/postconditioning could significantly reduce necrosis and apoptosis of ischemia/reperfusion myocardium. The mechanism of reducing the myocardial cell apoptosis may have relation to inhibiting the activation of pro-apoptotic gene caspase-3 and increased expression of Bcl-2.

Objective: In this study, we try to find the better protocol of limb ischemia postconditioning by observing different protective effects of limb ischemic postconditioning (different strength and time windows in rabbits)., Methods: 42 healthy New Zealand rabbits were randomly divided into 7 groups (n = 6): Sham; Control (CON); Skeletal muscle postconditioning (SP); 6 min-delayed skeletal muscle postconditioning (6M-DSP); 1 min-delayed skeletal muscle postconditioning (1M-DSP); Strengthen skeletal muscle postconditioning (SSP); Weakened skeletal muscle postconditioning (WSP). Acute ischemia/reperfusion (I/R) model was induced by 45 minutes occlusion on left circumflex coronary artery (LCX) and 2 hours reperfusion in all anesthetized open-chest rabbits except the Sham. Limb ischemia was induced by external iliac arteries occlusion and reperfusion through artery clamps. The extent of myocardial infarction was assessed by triphenyltetrazolium (TTC) staining. Blood serum creatine kinase (CK) activity and lactate dehydrogenase (LDH) activity were measured at baseline,the end of ischemia, after 1 hour and 2 hours of reperfusion respectively., Results: Compared with the CON, the weight ratio and area ratio of myocardial infarction size were significantly decreased by 49.97% and 43.78% in SP, by 42.32% and 42.68% in 1M-DSP, by 48.36% and 48.86% in SSP (P < 0.05). But there was no significant difference between SP and 1M-DSP and SSP (P > 0.05). Otherwise, compared with the CON, myocardial infarct size was not significantly reduced in 6M-DSP or WSP (P > 0.05). The change of CK was similar to the trend of myocardial infarct size., Conclusion: The limb ischemia strength of 5 mini/1 minR x 1 cycle could significantly reduce the myocardial ischemia/ reperfusion injury in rabbits, if it was achieved before myocardial reperfusion.