Effects of cold cardioplegia on pH, Na, and Ca in newborn rabbit hearts
Effects of cold cardioplegia on pH, Na, and Ca in newborn rabbit hearts
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DOI：
10.1152/ajpheart.00776.2004
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发表时间：
2006-03-01
影响因子：
4.8
通讯作者：
Cala, PM
中科院分区：
文献类型：
--
作者：
Anderson, SE;Liu, H;Cala, PM
许多研究表明，心肌缺血再灌注 (I/R) 损伤主要是由胞质质子 (Hi) 刺激的胞质 Na (Na-i) 增加引起的，这会导致 Na/Ca 交换介导的胞质 Ca 浓度 ([Ca](i)) 增加。由于冷晶体停跳液 (CCC) 限制了 [ H] i，我们测试了这样的假设：在新生儿心脏中，CCC 会减少 I/R 期间的 H-i、Na-i 和 Ca-i 积累，以限制损伤。 NMR 测量了离体 Langendorff 灌注的新生兔心脏中的细胞内 pH (pH(i))、Na-i、[Ca](i) 和 ATP。对照缺血方案为基线灌注30分钟，整体缺血40分钟，再灌注40分钟，均在37℃下。CCC方案相同，只是缺血前输注冰冷的CCC 5分钟，缺血期间心脏温度降至12℃。除温度外，正常钾 CCC 溶液 (NKCCC) 与对照灌注液相同；高钾 (HKCCC) 与 NKCCC 相同，只是用额外的 11 mmol/l KCl 等渗替代了 NaCl。 NKCCC 和 HKCCC 在任何测量中都没有显着差异。以下是不同的（P < 0.05）。 CCC 组的缺血终末 pHi 高于对照组。同样，CCC 在 I/R 期间限制了 Nai 的增加。对照组的缺血终末Nai值（以meq/kg干重计）为115+/-16，NKCCC组为49+/-13，HKCCC组为37+/-12。 CCC 还改善了再灌注期间的 [Ca]i 恢复。再灌注40分钟后，对照组[Ca]i值（nmol/l）为302±50，NKCCC组为145±13，HKCCC组为182±19。 CCC 限制了缺血期间 ATP 的消耗，改善了 ATP 的恢复，并在再灌注期间左心室产生压力并减少了肌酸激酶的释放。令人惊讶的是，CCC 在缺血期间并没有显着限制 [Ca](i)。后者被解释为冷却时细胞内缓冲液中 Ca 释放的结果。
Many studies suggest myocardial ischemia-reperfusion (I/R) injury results largely from cytosolic proton (Hi)-stimulated increases in cytosolic Na (Na-i), which cause Na/Ca exchange-mediated increases in cytosolic Ca concentration ([Ca](i)). Because cold, crystalloid cardioplegia (CCC) limits [ H] i, we tested the hypothesis that in newborn hearts, CCC diminishes H-i, Na-i, and Ca-i accumulation during I/R to limit injury. NMR measured intracellular pH (pH(i)), Na-i, [Ca](i), and ATP in isolated Langendorff-perfused newborn rabbit hearts. The control ischemia protocol was 30 min for baseline perfusion, 40 min for global ischemia, and 40 min for reperfusion, all at 37 C. CCC protocols were the same, except that ice-cold CCC was infused for 5 min before ischemia and heart temperature was lowered to 12 C during ischemia. Normal potassium CCC solution (NKCCC) was identical to the control perfusate, except for temperature; the high potassium (HKCCC) was identical to NKCCC, except that an additional 11 mmol/l KCl was substituted isosmotically for NaCl. NKCCC and HKCCC were not significantly different for any measurement. The following were different (P < 0.05). End-ischemia pHi was higher in the CCC than in the control group. Similarly, CCC limited increases in Nai during I/R. End-ischemia Nai values (in meq/kg dry wt) were 115 +/- 16 in the control group, 49 +/- 13 in the NKCCC group, and 37 +/- 12 in the HKCCC group. CCC also improved [ Ca] i recovery during reperfusion. After 40 min of reperfusion, [ Ca] i values ( in nmol/l) were 302 +/- 50 in the control group, 145 +/- 13 in the NKCCC group, and 182 +/- 19 in the HKCCC group. CCC limited ATP depletion during ischemia and improved recovery of ATP and left ventricular developed pressure and decreased creatine kinase release during reperfusion. Surprisingly, CCC did not significantly limit [Ca](i) during ischemia. The latter is explained as the result of Ca release from intracellular buffers on cooling.