Levitsky S, Feinberg H
Department of Surgery, Abraham Lincoln School of Medicine, University of Illinois College of Medicine, Chicago 60680.
Ann Thorac Surg. 1975 Jul;20(1):21-9. doi: 10.1016/s0003-4975(10)63846-5.
Normothermic ischemic arrest by aortic cross-clamping, a widely used clinical technique, is associated with metabolic changes in the myocardium that are incompletely understood. The effects of aortic cross-clamping on glycolytic pathways as well as associated morphological changes are discussed. Emphasis is placed on the conservation of high-energy phosphate moieties during the period of cross-clamping as well as during reperfusion. A marked reduction in total high-energy phosphates (62%) and glycogen (63%) and an increase in lactate production (243%) denote a shift to anaerobic metabolism during the period of arrest. Despite reperfusion, total high-energy nucleotides remained depressed. The data suggest that persistent abnormal myocardial carbohydrate metabolism and low levels of high-energy nucleotides prevent recovery of contractility following normothermic ischemic arrest and reperfusion.
通过主动脉交叉钳夹进行常温缺血性停搏是一种广泛应用的临床技术,它与心肌代谢变化相关,而这些变化尚未完全明确。本文讨论了主动脉交叉钳夹对糖酵解途径的影响以及相关的形态学变化。重点在于交叉钳夹期间以及再灌注期间高能磷酸基团的保存情况。在停搏期间,总高能磷酸盐(减少62%)和糖原(减少63%)显著降低,乳酸生成增加(增加243%),这表明代谢已转向无氧代谢。尽管进行了再灌注,总高能核苷酸水平仍持续降低。数据表明,常温缺血性停搏和再灌注后,持续异常的心肌碳水化合物代谢和低水平的高能核苷酸会阻碍心肌收缩力的恢复。