Cellular Protection during Myocardial Ischemia The Development and Characterization of a Procedure for the
Cellular Protection during Myocardial Ischemia The Development and Characterization of a Procedure for the
复制标题
心肌缺血期间的细胞保护 心肌缺血过程的开发和表征
作者：
D. Hearse;D. Stewart;M. Braimbridge;B. Chir.
摘要：本研究采用离体灌注大鼠心脏模型，观察各种保护剂单独使用或联合使用在多大程度上能够增加心脏对短暂性缺血的抵抗力。这项研究的目的是开发一种溶液，如果在心肌缺血发作之前将其注入冠状血管，将迅速诱导心肌骤停，并抵消心肌缺血期间已知发生的几种有害细胞变化。研究了诱发心脏骤停、改变细胞离子损失、影响底物利用、能量产生和能量储存、影响冠状血管直径和细胞肿胀、预防心律失常和影响代谢率的药物。评价了这些药剂的加性效应。配制了一种含有高浓度钾、镁、三磷酸腺苷、磷酸肌酸和普鲁卡因的水溶液。该溶液使缺血大鼠心脏（37°C 30 min）的恢复率从0%提高到93%。低温可以进一步延长缺血的安全时间。
SUMMARY An isolated perfused working rat heart model was used to investigate the extent to which various protective agents, used either singly or in combination, were able to increase the resistance of the heart to periods of transient ischemia. The aim of the studies was to develop a solution which, if infused into the coronary vessels just prior to the onset of ischemia, would rapidly induce arrest and would also counteract several of the deleterious cellular changes known to occur during myocardial ischemia. Agents which induce cardiac arrest, modify cellular ion loss, affect substrate utilization, energy production and energy stores, affect coronary vessel diameter and cell swelling, prevent dysrhythmias, and affect metabolic rate were investigated. The additive effects of these agents were evaluated. An aqueous solution was formulated which contained high concentrations of potassium and magnesium, in combination with adenosine triphosphate, creatine phosphate and procaine. This solution increased the recovery of the ischemic (37° C for 30 min) rat heart from 0% to 93%. The safe period of ischemia could be further increased by the use of hypothermia.