Yu T, Liu X, Yu Z, Yang S, Ye Y, Yang X, Gao Z
Department of Anesthesiology, Zunyi Medical College, Zunyi 563003, China.
Zhonghua Wai Ke Za Zhi. 2000 Dec;38(12):931-4.
To investigate the myocardial protective effects of pinacidil-induced hyperpolarized arrest and compare them with those induced with depolarized hyperkalemic arrest.
18 dogs were equally divided into three groups. In the hypothermic hyperpolarization group (LH group), after aortic cross-clamping, a single dose of 4 degrees C pinacidil containing St. Thomas cardioplegic was infused through the aortic root. Temperature during CPB was kept between 26 - 28 degrees C and warmed to 37 degrees C before aortic declamping. Global ischemia lasted 60 min and then reperfusion started for 30 min. In the normothermic hyperpolarized group (WH group), the same procedure was set as in the LH group, except maintaining temperature of 35 - 37 degrees C for CPB and pinacidil solution. In the control group (group C), no pinacidil in St. Thomas solution was the only difference to the other 2 groups. Cardiac arrest and its recovery, the ultrastructure of the myocardium and hemodynamic during ischemia and after reperfusion were observed in the 3 groups.
(1) The percentages of normal mitochondria and glycogen were not changed significantly during ischemia and after reperfusion in the LH group, but declined markedly in the group C at ischemic 30, 60 min, and reperfusion for 20 min (P < 0.01). In the WH group, they were lower than those of the group LH, but higher than those of the group C before ischemia. (2) The recoveries of CO, SV, CI, LVSW, RVSW, MAP in the LH group were significantly better than those in the other two groups after reperfusion for 15 minutes and 30 minutes (P < 0.05 or 0.01). However, they were much better in the WH group than in the group C (P < 0.05 or 0.01). (3) The time from cardioplegic infusion to cardiac arrest was shorter in the group C and the group LH than in the group WH.
Myocardial protection for global ischemia during CPB could be well achieved with hyperpolarized cardiac arrest induced by ATP-sensitive potassium channel opener, pinacidil, especially in the hypothermic state. The protection is weaker in normothermia but is still stronger than that with traditional depolarized arrest.
研究吡那地尔诱导的超极化停搏的心肌保护作用，并与去极化高钾停搏的心肌保护作用进行比较。
将18只犬平均分为三组。低温超极化组（LH组），在主动脉阻断后，经主动脉根部注入含4℃吡那地尔的圣托马斯心脏停搏液。体外循环期间温度维持在26 - 28℃，在主动脉开放前升温至37℃。全心缺血持续60分钟，然后开始再灌注30分钟。常温超极化组（WH组），除体外循环和吡那地尔溶液温度维持在35 - 37℃外，其余操作同LH组。对照组（C组），圣托马斯溶液中不含吡那地尔，这是与其他两组的唯一区别。观察三组的心脏停搏及其恢复情况、心肌超微结构以及缺血和再灌注期间的血流动力学。
（1）LH组缺血及再灌注期间正常线粒体和糖原的百分比无明显变化，但C组在缺血30、60分钟及再灌注20分钟时显著下降（P < 0.01）。WH组在缺血前低于LH组，但高于C组。（2）再灌注15分钟和30分钟后，LH组的CO、SV、CI、LVSW、RVSW、MAP恢复情况明显优于其他两组（P < 0.05或0.01）。然而，WH组也明显优于C组（P < 0.05或0.01）。（3）C组和LH组从心脏停搏液注入到心脏停搏的时间比WH组短。
通过ATP敏感性钾通道开放剂吡那地尔诱导的超极化停搏可很好地实现体外循环期间全心缺血的心肌保护，尤其是在低温状态下。常温时保护作用较弱，但仍强于传统的去极化停搏。
