Schepkin V D, Choy I O, Budinger T F, Young J N, DeCampli W M
Center for Functional Imaging, Lawrence Berkeley National Lab, Berkeley, CA, USA.
J Mol Cell Cardiol. 1999 Sep;31(9):1643-51. doi: 10.1006/jmcc.1999.1002.
The goal of this study was to assess the effect of multi-dose St Thomas' cardioplegia on intracellular sodium homeostasis in a rat heart model. A new magnetic resonance method was applied which enable us to detect intracellular Na changes without chemical shift reagents. Three groups of isolated rat hearts were subjected to 51 min of ischemia and 51 min of reperfusion at 37 degrees C: Group 1-three infusions of St Thomas' cardioplegia every 17 min for 2 min (n=7); Group 2-single-dose infusion of cardioplegia at the beginning of stop-flow ischemia (n=8); and Group 3-clamp ischemia (n=3) without cardioplegia administration. Performance of the heart was assessed by rate-pressure product relative to the pre-ischemic level (RPP). An NMR method was applied which continuously detects the Na(i) concentration in the heart, using the ability of bound sodium to exhibit triple-quantum transitions and the growth of the corresponding signal when sodium ions pass from extracellular to intracellular space. Clamp ischemia without cardioplegia and 50 min of reperfusion left the heart dysfunctional, with Na(i) growth from the pre-ischemic level of 13.9+/-1.2 mM to 34.9+/-1.3 mM and 73. 9+/-1.9 mM at the end of ischemia and reperfusion, respectively. During single-dose cardioplegia the corresponding values for Na(i) were 30.2+/-1 mM and 48.5+/-1.7 mM (RPP=29%). Multiple infusions of cardioplegic solution resulted in a remarkable preservation of the heart's intracellular Na concentration with a non-significant increase in Na(i) during ischemia and only 16.7+/-1 mM, (P=0.01), after subsequent reperfusion (RPP=85%). The time course of Na(i) changes in the rat heart model demonstrates a prominent potential of multi-dose St Thomas' cardioplegia in preserving intracellular sodium homeostasis at 37 degrees C. The growth of Na(i) concentration during ischemia, as an indicator of the viability of the myocytes, can have a prognostic value for the heart's performance during reperfusion.
本研究的目的是在大鼠心脏模型中评估多剂量圣托马斯心脏停搏液对细胞内钠稳态的影响。应用了一种新的磁共振方法,该方法使我们能够在不使用化学位移试剂的情况下检测细胞内钠的变化。三组离体大鼠心脏在37℃下经历51分钟的缺血和51分钟的再灌注:第1组,每17分钟输注3次圣托马斯心脏停搏液,每次2分钟(n = 7);第2组,在停流缺血开始时单次输注心脏停搏液(n = 8);第3组,钳夹缺血(n = 3),不给予心脏停搏液。通过相对于缺血前水平的心率-压力乘积(RPP)评估心脏功能。应用了一种核磁共振方法,该方法利用结合钠表现出三量子跃迁的能力以及当钠离子从细胞外空间进入细胞内空间时相应信号的增长来连续检测心脏中的细胞内钠浓度(Na(i))。无心脏停搏液的钳夹缺血和50分钟的再灌注使心脏功能失调,缺血结束时和再灌注结束时细胞内钠浓度分别从缺血前的13.9±1.2 mM增长至34.9±1.3 mM和73.9±1.9 mM。在单次剂量心脏停搏液处理期间,细胞内钠浓度的相应值分别为30.2±1 mM和48.5±1.7 mM(RPP = 29%)。多次输注心脏停搏液可显著维持心脏细胞内钠浓度,缺血期间细胞内钠浓度无显著增加,后续再灌注后仅为16.7±1 mM(P = 0.01)(RPP = 85%)。大鼠心脏模型中细胞内钠浓度变化的时间进程表明,多剂量圣托马斯心脏停搏液在37℃下维持细胞内钠稳态方面具有显著潜力。缺血期间细胞内钠浓度的增长作为心肌细胞活力的指标,可能对再灌注期间心脏的功能具有预后价值。