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目的 探讨 ATP敏感性钾通道开放剂 (KCOs) Pinacidil (5 0μmol/ L )对 L angendorff灌注兔心模型超极化停跳的保护作用。方法 选用离体兔心脏 2 4个 ,随机分成 3组 :对照组 (C组 ) ;低温超极化组 (L H组 ) ;常温超极化组 (WH组 )。离体兔心 L angendorff模型灌注充氧的 Krebs- Henseleit (K- H)液稳定后 ,L H组或 WH组分别灌注含 Pinacidil的 4℃或 37℃的 St.Thomas(K+ 5 m mol/ L )停跳液 ,C组为不含 Pinacidil的 St.Thom as (K+ 16 m mol/ L )停跳液。全心脏缺血 40 m in,复灌 2 0 min。结果 L H组心脏停跳迅速 ,WH组停跳缓慢 ,但复跳迅速 ,与 C组比较 ,差异有显著性 (P<0 .0 1) ;再灌注后 L H组心率的恢复较慢 ,与 WH组一样 ,心肌收缩力与左心内压的恢复显著快于 C组 (P<0 .0 5 ) ;L H组与 WH组心肌组织ATP、总腺苷量 (TAN)、细胞能荷 (EC)显著高于 C组 ,而丙二醛 (MDA)的含量明显低于 C组 (P<0 .0 5或 0 .0 1)。结论 Pinacidil 5 0μm ol/ L诱导心脏超极化停跳 ,能够降低心肌 ATP的消耗 ,减少脂质过氧化物的形成 ,明显改善离体兔心缺血 /再灌注后期心功能
Objective To investigate the protective effect of Pinacidil (50 μmol / L), an ATP-sensitive potassium channel opener, on hyperpolarized arrest in Langentorff perfusion rabbit heart model. Methods 24 rabbits were randomly divided into 3 groups: control group (C group), hypothermia hyperpolarization group (L H group) and normal temperature hyperpolarization group (WH group). After instillation of Krebs-Henseleit (K-H) solution of isolated rabbit heart Langendorff model, the LH group or WH group were respectively perfused with Pinacidil at 4 ° C or 37 ° C for St. Thomas (K + 5 m mol / L) The patients in Group C were St.Thom as (K + 16 m mol / L) with no Pinacidil. Whole heart ischemia 40 m in, reperfusion 20 min. Results The cardiac arrest was rapid in LH group, the arrest was slow in WH group, but rapidly rebounded, which was significantly different from that in C group (P <0.01). The HR recovery in LH group was slower than that in WH group In the same way, the recovery of myocardial contractility and left ventricular pressure was significantly faster than that of group C (P <0.05). The levels of ATP, TAN and EC in LH and WH group were significantly higher than those in C group The content of malondialdehyde (MDA) in group C was significantly lower than that in group C (P <0.05 or 0.01). Conclusions Pinacidil induced cardiac hyperpolarization and cardioplegia in the presence of 50μmol / L, which can reduce myocardial ATP consumption and lipid peroxidation, and significantly improve cardiac function in isolated rabbit heart after ischemia / reperfusion