Cohen N M, Allen C A, Hsia P W, Nixon T E, Wise R M, Damiano R J
Department of Surgery, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0068.
Ann Thorac Surg. 1994 May;57(5):1076-83. doi: 10.1016/0003-4975(94)91332-3.
Myocardial protection strategies use cardioplegic solutions to reduce the injury induced by surgical ischemia and reperfusion. However, there is a high incidence of electrophysiologic abnormalities after cardioplegic arrest. A computerized epicardial mapping system in a porcine cardiopulmonary bypass model was used to measure the electrophysiologic consequences of different myocardial protection techniques. Both warm and cold, crystalloid and blood cardioplegic solutions were compared. The effects of hypothermia and prolonged cardiopulmonary bypass were examined in a control group that underwent a 2-hour period of hypothermia without cardioplegia or aortic cross-clamping, followed by 2 hours of normothermic reperfusion. Isochronous activation maps, unipolar electrograms, ventricular refractory periods, and pacing thresholds were measured before cardioplegic arrest and during reperfusion. Compared with the control group, crystalloid cardioplegia, but not blood cardioplegia, was accompanied by large changes in the pattern of ventricular activation and by persistent (> 2 hours) and significant slowing of the time required for complete ventricular activation. This was not the result of hypoxia. Moreover, the effective refractory period and the pacing threshold were unchanged by any cardioplegia. Our data suggest that crystalloid cardioplegia increases myocardial resistance to current flow leading to a derangement of electrical impulse propagation that may underlie arrhythmogenesis.
心肌保护策略使用心脏停搏液来减少手术缺血和再灌注所导致的损伤。然而，心脏停搏后电生理异常的发生率很高。在猪体外循环模型中使用计算机化的心外膜标测系统来测量不同心肌保护技术的电生理后果。比较了温血和冷血、晶体和含血心脏停搏液。在一个对照组中检查了低温和长时间体外循环的影响，该对照组经历了2小时的低温但未进行心脏停搏或主动脉阻断，随后进行2小时的常温再灌注。在心脏停搏前和再灌注期间测量了等时激活图、单极电图、心室不应期和起搏阈值。与对照组相比，晶体心脏停搏液（而非含血心脏停搏液）伴随着心室激活模式的巨大变化以及持续（>2小时）且显著减慢的完全心室激活所需时间。这不是缺氧的结果。此外，任何心脏停搏液都未改变有效不应期和起搏阈值。我们的数据表明，晶体心脏停搏液增加了心肌对电流的阻力，导致电冲动传播紊乱，这可能是心律失常发生的基础。
