Myocardial protection in the acutely injured heart: hyperpolarizing versus depolarizing hypothermic cardioplegia.
Myocardial protection in the acutely injured heart: hyperpolarizing versus depolarizing hypothermic cardioplegia.
复制标题
急性损伤心脏的心肌保护：超极化与去极化低温停跳液。
DOI：
10.1016/s0022-5223(97)70372-6
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发表时间：
1997
期刊：
影响因子：
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通讯作者：
DamianoJr,RJ
中科院分区：
文献类型：
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作者：
Lawton,JS;Hsia,PW;Allen,CT;DamianoJr,RJ
目的 在常温缺血期间，使用三磷酸腺苷敏感钾通道开放剂进行超极化骤停优于标准高钾去极化心脏停搏液已被证实。本研究检验了吡那地尔在临床上更相关的急性损伤心脏和低温心脏停搏骤停模型中提供卓越保护的假设。方法在血液灌注、共生、兔心 Langendorff 模型中，心脏经历 15 分钟无保护的全身常温缺血，然后在 4°C 下给予 50 ml 心脏停搏液，然后进行 50 分钟低温 (15°C) 缺血和 30 分钟再灌注。所施用的心脏停搏液由单独的 Krebs-Henseleit 溶液 (N = 6)、含有吡那地尔的 Krebs-Henseleit 溶液 (50 μmol/L；N = 10)、含有吡那地尔 (50 μmol/L) 和格列本脲（一种钾通道阻滞剂，10 μmol/L；N = 8）的 Krebs-Henseleit 溶液或圣托马斯医院溶液 (N = 8) 组成。 8).比较了形成压力的恢复百分比、线性舒张压-容量关系和冠脉血流量。 结果 对于 Krebs-Henseleit、含有吡那地尔和吡那地尔的 Krebs-Henseleit，形成压力的恢复百分比分别为 32.8% ± 2.8%、43.0% ± 4.3%、46.5% ± 2.2% 和 49.3% ± 2.7%。分别使用格列本脲、圣托马斯医院和 Krebs-Henseleit 联合吡那地尔组。再灌注时没有心脏出现心室颤动。结论与我们之前研究中的常温缺血相反，在低温超极化骤停期间，与传统高钾骤停期间的结果相比，心室颤动的发生率既没有增加，电活动也没有延长。圣托马斯医院溶液和吡那地尔的心肌保护优于单独使用 Krebs-Henseleit 溶液 (p = 0.009)。添加格列本脲后，吡那地尔提供的保护作用消失，表明该药物在低温期间具有三磷酸腺苷敏感的钾通道活性。 (胸心血管外科杂志 1997 年；113:567-75)
ObjectivesThe superiority of hyperpolarized arrest with adenosine triphosphate–sensitive potassium channel openers over standard hyperkalemic depolarizing cardioplegia during normothermic ischemia has been documented. This study examined the hypothesis that pinacidil would provide superior protection in a more clinically relevant model of an acutely injured heart and hypothermic cardioplegic arrest.MethodsIn a blood-perfused, parabiotic, rabbit heart Langendorff model, hearts underwent 15 minutes of unprotected global normothermic ischemia before the administration of 50 ml of cardioplegic solution at 4° C, followed by 50 minutes of hypothermic (15° C) ischemia and 30 minutes of reperfusion. The cardioplegic solutions administered consisted of Krebs-Henseleit solution alone (N = 6), Krebs-Henseleit solution with pinacidil (50 μmol/L; N = 10), Krebs-Henseleit solution with pinacidil (50 μmol/L) and glibenclamide (a potassium channel blocker, 10 μmol/L; N = 8), or St. Thomas' Hospital solution (N = 8). The percent recovery of developed pressure, linear diastolic pressure-volume relationships, and coronary blood flow were compared.ResultsThe percent recovery of developed pressure was 32.8% ± 2.8%, 43.0% ± 4.3%, 46.5% ± 2.2%, and 49.3% ± 2.7% for the Krebs-Henseleit, the Krebs-Henseleit with pinacidil and glibenclamide, the St. Thomas' Hospital, and the Krebs-Henseleit with pinacidil groups, respectively. No hearts had ventricular fibrillation on reperfusion.ConclusionsDuring hypothermic hyperpolarized arrest, as opposed to normothermic ischemia as in our previous studies, there was neither an increased incidence of ventricular fibrillation nor prolonged electrical activity when compared with results during traditional hyperkalemic arrest. Myocardial protection by St. Thomas' Hospital solution and pinacidil was superior (p = 0.009) to that with Krebs-Henseleit solution alone. The protection provided by pinacidil was lost with the addition of glibenclamide, indicating that the drug has adenosine triphosphate–sensitive potassium channel activity during hypothermia. (J Thorac Cardiovasc Surg 1997;113:567-75)