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目的探讨尼可地尔药物预处理、后处理及二者联合对离体大鼠心肌缺血再灌注损伤的冠脉流出液生化指标、心肌梗死面积的影响,为临床缺血再灌注损伤的治疗提供理论依据。方法45只大鼠随机分为5组,离体心脏Langendorff装置灌流,(1)对照组(Con):左冠前降支(LAD)阻断40 min,复灌120 min。(2)预处理组(Ipc):在LAD阻断前先给予10 min的尼可地尔(Nic)20μmol/L。(3)后处理组(Npo):于复灌时给予10 min Nic。(4)联合组(Npp):LAD阻断前后分别给予Nic。(5)阻滞剂组(Gnp):灌注液中含有格列本脲(Gli)20μmol/L。结果Ipc、Npo、Npp同Con比较,CF在复灌后各时间点增高(P<0.05),Gnp同Con比较差异无统计学意义(P>0.05)。Npp同Ipc、Npo比较未表现出叠加效应(P>0.05)。复灌30 min后Ipc、Npo、Npp中CK、LDH漏出量较少(P<0.05),Con同Gnp比较差异无统计学意义,Npp同Ipc、Npo比较差异无统计学意义。Ipc中心肌梗死区重量从(50.02±2.90)%下降到(22.72±3.60)%,Npp和Npo梗死重量分别减小到(23.99±4.30)%和(29.02±2.10)%(P<0.05),Gli取消了Nic的保护作用,心肌梗死重量为(46.82±6.70)%(P>0.05)。结论尼可地尔预处理、后处理及二者联合对离体大鼠心肌有保护作用,但二者联合未表现明显叠加作用。尼可地尔后处理的心肌保护效应可能与再灌注早期的K-ATP通道的激活密切相关。
Objective To investigate the effects of nicorandil pretreatment, post-treatment and biochemical parameters of coronary effluent and myocardial infarct size in isolated rat myocardial ischemia-reperfusion injury in order to provide a basis for the treatment of clinical ischemia-reperfusion injury Provide a theoretical basis. Methods 45 rats were randomly divided into 5 groups. Langendorff apparatus was used to perfuse the isolated heart. (1) Control group (Con): occlusion of left anterior descending coronary artery (LAD) for 40 min and reperfusion for 120 min. (2) Pretreatment group (Ipc): Nicorandil (Nic) 20 μmol / L was given for 10 min before LAD blockade. (3) Post-treatment group (Npo): given 10 min Nic during reperfusion. (4) Combination group (Npp): Nicotidine was administered before and after LAD blockade. (5) Blockers group (Gnp): perfusate containing glibenclamide (Gli) 20μmol / L. Results Compared with Con, Ipc, Npo and Npp increased CF at each time point after reperfusion (P <0.05). There was no significant difference between Gnp and Con (P> 0.05). There was no additive effect between Npp and Ipc, Npo (P> 0.05). The leakage of CK and LDH in Ipc, Npo and Npp after reperfusion for 30 min was less (P <0.05), while the difference between Con and Gnp was not statistically significant. There was no significant difference between Npp and Ipc and Npo. The weight of infarct in Ipc decreased from (50.02 ± 2.90)% to (22.72 ± 3.60)%, and the weight of Npp and Npo decreased to (23.99 ± 4.30)% and (29.02 ± 2.10)% Gli canceled the protective effect of Nic, myocardial infarction weight (46.82 ± 6.70)% (P> 0.05). Conclusions Nicorandil preconditioning, post-treatment and their combination have protective effects on isolated rat myocardium, but the combination of the two does not show obvious superposition. Myocardial protective effect of nicorandil postconditioning may be closely related to the activation of K-ATP channel in the early stage of reperfusion.