Liu X, Engelman R M, Rousou J A, Flack J E, Deaton D W, Das D K
Cardiovascular Division, University of Connecticut School of Medicine, Farmington.
Circulation. 1994 Nov;90(5 Pt 2):II316-20.
Development of intracellular calcium overloading is to be a primary factor in cellular injury during myocardial reperfusion. We studied the effects of different temperatures during continuously perfused cardioplegic arrest on the changes of intracellular calcium concentration ([Ca2+]i) level in isolated rat hearts.
Rat hearts were perfused by the Langendorff technique with Krebs-Henseleit bicarbonate (KHB) buffer. The [Ca2+]i was monitored by loading the heart with fura-2 acetoxymethyl ester and by using a [Ca2+]i analyzer. [Ca2+]i was calculated by determining the maximal and minimal fluorescent intensity for each heart. The hearts (n = 6 in each group) were subjected to cardioplegic arrest by continuous perfusion of oxygenated crystalloid K+ (15 mEq/L) cardioplegic solution (CPS) at different temperatures (4 degrees C, 20 degrees C, 28 degrees C, 37 degrees C) for 120 minutes, followed by 30 minutes of normothermic KHB buffer reperfusion. A fifth group received continuous perfusion as a control with 37 degrees C KHB buffer. The baseline values of [Ca2+]i were comparable in all experimental groups. In hearts perfused with 4 degrees C CPS, [Ca2+]i increased significantly during reperfusion (from 221 +/- 24 nmol/L [mean +/- SEM] at baseline to 341 +/- 19 at the end of reperfusion, P < .05). CPS perfusion at 20 degrees C also induced significant Ca2+ overloading during reperfusion, but not as much as in the 4 degrees C group. No significant [Ca2+]i increase occurred at 28 degrees C or 37 degrees C.
Continuous cardioplegic perfusion at lower temperatures (ie, 4 degrees C or 20 degrees C) induces Ca2+ overloading during reperfusion, which is detrimental to the optimal recovery of ventricular performance, while normothermic cardioplegic perfusion prevents the development of Ca2+ accumulation. These results provide experimental evidence for a detrimental effect of prolonged hypothermic continuous cardioplegia.
细胞内钙超载的发生是心肌再灌注期间细胞损伤的主要因素。我们研究了持续灌注心脏停搏期间不同温度对离体大鼠心脏细胞内钙浓度（[Ca2+]i）水平变化的影响。
采用Langendorff技术用Krebs-Henseleit碳酸氢盐（KHB）缓冲液灌注大鼠心脏。通过用fura-2乙酰氧基甲酯加载心脏并使用[Ca2+]i分析仪监测[Ca2+]i。通过确定每个心脏的最大和最小荧光强度来计算[Ca2+]i。心脏（每组n = 6）在不同温度（4℃、20℃、28℃、37℃）下通过持续灌注含氧晶体K+（15 mEq/L）心脏停搏液（CPS）120分钟进行心脏停搏，随后进行30分钟的常温KHB缓冲液再灌注。第五组接受37℃KHB缓冲液持续灌注作为对照。所有实验组的[Ca2+]i基线值相当。在用4℃CPS灌注的心脏中，再灌注期间[Ca2+]i显著增加（从基线时的221±24 nmol/L[平均值±标准误]增加到再灌注结束时的341±19，P <.05）。20℃下的CPS灌注在再灌注期间也诱导了显著的钙超载，但不如4℃组严重。在28℃或37℃时未发生显著的[Ca2+]i增加。
较低温度（即4℃或20℃）下的持续心脏停搏灌注在再灌注期间诱导钙超载，这对心室功能的最佳恢复有害，而常温心脏停搏灌注可防止钙积累的发生。这些结果为长时间低温持续心脏停搏的有害作用提供了实验证据。
