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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rh BNP(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rh BNP,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)、c Tn I(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、c Tn I和CK-MB水平:BNP组与AMI组比较,MDA、c Tn I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、c Tn I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。
Objective: Protective effect of brain natriuretic peptide postconditioning on acute myocardial infarction in rabbits and its possible mechanism. Methods: Thirty rabbits were randomly divided into 3 groups with 10 rats in each group. The left coronary arteries were occluded for 30 minutes and reperfused for 120 minutes. AMI (acute myocardial infarction) group: saline infusion during reperfusion; BNP (brain natriuretic peptide) group: rh BNP (recombinant human brain natriuretic peptide) was intravenously dripped during reperfusion; BNP + GLY Peptide + glibenclamide) group: rh BNP was intravenously injected during reperfusion, while GLY was injected sublingually. The changes of ECG were monitored continuously. The incidence of ventricular fibrillation (VF) and ventricular tachycardia (VT) were measured 120 min after reperfusion. After myocardial reperfusion for 120 min, SOD, MDA, cTn I (troponin I) and CK-MB (creatine kinase isoenzyme) were determined. Each group were randomly selected 2 rabbits, respectively, at 1 hour and 2 hours after reperfusion apex organization, HE staining. Results: (1) Reperfusion arrhythmia: Compared with AMI group, the incidence of VT and VF were significantly increased in BNP group (all P <0.01); the incidence of VT and VF in BNP + GLY group was significantly higher than that in BNP group (All P <0.01). (2) The levels of SOD, MDA, cTn I and CK-MB: Compared with AMI group, the levels of MDA, cTn I and CK-MB were significantly decreased (all P <0.01) <0.01). Compared with BNP group, the levels of MDA, cTn I and CK-MB in BNP + GLY group were significantly increased (P <0.01, P <0.05 and P <0.01, respectively) ). (3) HE staining of myocardium: Myocardial injury was obvious in AMI group and BNP + GLY group, and myocardial injury in BNP group was slight. CONCLUSION: Brain natriuretic peptide post-treatment has a protective effect on acute myocardial infarction (ischemia-reperfusion injury) in rabbits, which may be related to KATP channel.