NORMOTHERMIC CARDIOPLEGIA PREVENTS INTRACELLULAR CALCIUM ACCUMULATIONDURING CARDIOPLEGIC ARREST AND REPERFUSION

Background Development of intracellular calcium overloading is to be a primary factor in cellular injury during myocardial reperfusion. We s tudied the effects of different temperatures during continuously perfu sed cardioplegic arrest on the changes of intracellular calcium concen tration ([Ca2+](i)) level in isolated rat hearts. Methods and Results Rat hearts were perfused by the Langendorff technique with Krebs-Hense leit bicarbonate (KHB) buffer. The [Ca2+](i) was monitored by loading the heart with fura-2 acetoxymethyl ester and by using a [Ca2+]i analy zer. [Ca2+](i) was calculated by determining the maximal and minimal f luorescent intensity for each heart. The hearts (n=6 in each group) we re subjected to cardioplegic arrest by continuous perfusion of oxygena ted 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 rep erfusion. A fifth group received continuous perfusion as a control wit h 37 degrees C KHB buffer. The baseline values of [Ca2+](i) were compa rable 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 reperfusi on, 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. Conclusions Continuous cardioplegic perfusion at lower temperatures (ie, 4 degrees C or 20 degrees C) induces Ca2+ overloadin g during reperfusion, which is detrimental to the optimal recovery of ventricular performance, while normothermic cardioplegic perfusion pre vents the development of Ca2+ accumulation. These results provide expe rimental evidence for a detrimental effect of prolonged hypothermic co ntinuous cardioplegia.