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目的：脑利钠肽后处理对兔急性心肌梗死的保护作用及可能机制。方法：30 只兔随机分为3 组，每组10 只，左冠状动脉的左室支缺血30 分钟，再灌注120 分钟。AMI（急性心肌梗死）组：再灌注期间静脉滴注生理盐水；BNP（脑利钠肽）组：再灌注期间静脉滴注rhBNP(重组人脑利钠肽)；BNP+GLY（脑利钠肽+格列苯脲）组：再灌注期间静脉滴注rhBNP，同时舌下静脉注射GLY 。连续监测心电变化，统计再灌注120 min 室性心动过速(VT)、心室颤动(VF)的发生率。心肌再灌注120 min 后，分别测定SOD(超氧化物歧化酶)、MDA（丙二醛）、cTnI（肌钙蛋白I）、CK-MB（肌酸激酶同工酶）。各组随机抽取2 只兔，分别于再灌注1 小时和2 小时末取心尖组织，HE 染色。结果：（1）再灌注心律失常：BNP 组与AMI组比较，VT 和VF发生率均明显升高（均为P<0.01）；BNP+GLY 组与BNP 组比较，VT 和VF 发生率均明显升高（均为P<0.01）。（2）SOD、MDA、cTnI 和CK-MB 水平：BNP 组与AMI 组比较， MDA、cTnI 和CK-MB 均明显降低（均为P<0.01），而SOD 明显升高（P<0.01）；BNP+GLY 组与BNP 组比较，MDA、cTnI 和 CK-MB 均明显升高（分别为P<0.01，P<0.05和P<0.01），而SOD明显降低（P<0.01）。（3）心肌HE 染色：AMI组和BNP+GLY 组心肌损伤明显，BNP 组心肌损伤轻微。结论：脑利钠肽后处理对兔急性心肌梗死（缺血- 再灌注损伤）具有保护作用，可能与KATP 通道相关。

英文摘要:

Objective:To study the protective effect of BNP postcondition on rabbits acute myocardial infarction and the mechanism.Methods:Thirty rabbits were randomly divided into three groups (n=10): AMI group (saline), BNP group (BNP), BNP+GLY group (BNP+GLY). The myocardial ischemia-reperfusion models were induced by 30 min coronary artery ligature and 120 min reperfusion in rabbits. The rabbits were given intravenous infusion according to the above methods during 120 min reperfusion. Arrhythmias were observed during 120 min reperfusion; the concentration of SOD, MDA, cTnI and CK-MB in plasma were measured at the end of reperfusion; meanwhile, the myocardial tissue was observed in optics microscope.Results:(1) Arrhythmia: In BNP group, the incidence of VT and VF were significantly lower than those in AMI group (both P<0.01); In BNP+GLY group, the above variables were significantly higer than those in BNP group (both P<0.01). (2) SOD, MDA, cTnI and CK-MB: In BNP group, the levels of MDA, cTnT and CK-MB were lower, but the activity of SOD was higer than those in AMI group (all P<0.01). Howerer, in BNP+GLY group, the above effects of BNP were blocked by GLY (P<0.01, P<0.05, P<0.01 and P<0.01 vs BNP group, respectively). (3) The myocardial tissue in optics microscope: the injuries of AMI and AMI+GLY group were worse than BNP group.Conclusion:These results suggest that BNP postcondition has cardioprotection effect on AMI in rabbits, which may be related to inhibition of KATP channel-GLY.

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