冠心康对豚鼠缺血再灌注心室乳头肌电生理特性的影响

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目的观察中药复方冠心康对豚鼠模拟缺血再灌注损伤心室乳头肌细胞电生理作用,初步探讨其心肌保护机制。方法将32只豚鼠随机分为模型组、格列苯脲组、吡那地尔组、冠心康组(每组8只),分离左心室乳头肌标本。模型组于正常台氏液平衡灌流30min后,用模拟缺血缺氧液灌流15min,再用正常台氏液复灌30min。吡那地尔组(100μmol/L)和格列苯脲组(100μmol/L)缺血前行药物预处理,其余步骤同模型组。冠心康组动物预先灌胃给予冠心康溶液生药6g.kg-1.d-1,每日1次,连续14日,然后分离左心室乳头肌,其余步骤同模型组。采用细胞内标准玻璃微电极技术记录各组动物心室乳头肌细胞电生理参数的变化。结果冠心康预处理对平衡期心肌无明显影响;进一步缩短了缺血早期5min和再灌注早期1min心肌90%动作电位时程(action potential duration at90%repolarization,APD90),与模型组比较有明显差异(P<0.05);自再灌注5min起,冠心康组心肌动作电位时程(action potential duration,APD)迅速恢复,至再灌注30min时50%动作电位时程(action potential duration at50%repo-larization,APD50)和APD90明显长于平衡期(P<0.05);冠心康对各时期心肌静息电位(resting potential,RP)、动作电位振幅(ac-tion potential amplitude,APA)均无明显影响。吡那地尔明显缩短缺血5min、再灌注1min、5min和10min心肌APD50和APD90,与模型组比较有显著差异(P<0.05),而格列苯脲则明显延长缺血和再灌注心肌APD。结论中药复方冠心康对缺血再灌注心肌细胞具有一定的保护作用,其电生理作用可能与影响KATP通道(ATP-sensitive potassium channels,KATP channels)和Ca2+通道有关。 Objective To observe the electrophysiological effects of Guanxinkang, a traditional Chinese medicine compound, on the ventricular papillary muscle cells in guinea pigs subjected to simulated ischemia-reperfusion injury and to explore its myocardial protective mechanism. Methods Thirty-two guinea pigs were randomly divided into model group, glibenclamide group, pinacidil group and Guanxinkang group (8 in each group). Left ventricular papillary muscle samples were isolated. The rats in model group were perfused with simulated hypoxic-ischemic anoxemia for 30 minutes after normal infusion of normal Tyrode’s solution for 30 minutes and re-injected with normal Tyrode’s solution for 30 minutes. Pinacidil group (100μmol / L) and glibenclamide group (100μmol / L) preconditioning ischemic preconditioning, the rest of the steps with the model group. Guanxinkang group was given gavage 6g.kg-1.d-1 once a day for 14 consecutive days, then isolated left ventricular papillary muscle, the rest of the steps with the model group. Intracellular standard glass microelectrode technique was used to record changes of electrophysiological parameters of ventricular papillary muscle cells in each group. Results Guanxinkang pretreatment had no significant effect on the myocardial cells during the equilibration period, and further shortened the 90% action potential duration at 90% repolarization (APD90) at 5 min in early ischemia and 1 min after reperfusion, (P <0.05). From 5 min after reperfusion, the myocardial electrophysiological potential duration (APD) of Guanxinkang group recovered rapidly, and the action potential duration at 50% repo -larization, APD50 and APD90 were significantly longer than those in the equilibrium period (P <0.05). Guanxinkang had no significant effect on resting potential (RP) and ac-tion potential amplitude (APA) . Pinacidil significantly shortened ischemia 5min, reperfusion 1min, 5min and 10min myocardial APD50 and APD90, compared with the model group were significantly different (P <0.05), while glibenclamide significantly prolonged ischemia and reperfusion myocardial APD . Conclusion Guanxinkang, a traditional Chinese medicine compound, may have a protective effect on myocardial cells during ischemia-reperfusion. Its electrophysiological effects may be related to the effects of KATP channels and Ca2 + channels.
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