Nayler W G
Eur Heart J. 1983 May;4 Suppl C:33-41. doi: 10.1093/eurheartj/4.suppl_c.33.
Irrespective of age or species, injured cardiac myocytes accumulate Ca2+. In this paper four different aspects of the Ca2+-overloading phenomenon are discussed. These aspects include the conditions under which it occurs, the possible routes of Ca2+ entry, the metabolic consequences of the raised tissue Ca2+ and possible protective procedures. The particular protective procedures that will be described involve the combined use of hypothermia and nifedipine (50 micrograms/l), with and without K+-induced chemical cardioplegia. Isolated, electrically paced rabbit hearts were made ischaemic for 60 to 180 min at 37, 28, 25, 15, 12 and 5 degrees C and then reperfused at 37 degrees C. In some experiments nifedipine was added to the perfusion buffer, with and without K+-induced cardioplegia. Recovery was assessed in terms of recovery of mechanical function, maintenance of the tissue stores of adenosine 5'-triphosphate (ATP) and creatine phosphate, and maintenance of the ATP-generating activity of the mitochondria. These results show that the cardioprotective effects of nifedipine and hypothermia are additive.
无论年龄或物种如何，受损的心肌细胞都会积累钙离子。本文讨论了钙离子过载现象的四个不同方面。这些方面包括其发生的条件、钙离子进入的可能途径、组织钙离子升高的代谢后果以及可能的保护措施。将描述的特定保护措施包括联合使用低温和硝苯地平（50微克/升），有无钾诱导的化学心脏停搏。将离体、电起搏的兔心脏在37、28、25、15、12和5摄氏度下缺血60至180分钟，然后在37摄氏度下再灌注。在一些实验中，无论有无钾诱导的心脏停搏，都将硝苯地平添加到灌注缓冲液中。通过机械功能的恢复、三磷酸腺苷（ATP）和磷酸肌酸的组织储备的维持以及线粒体ATP生成活性的维持来评估恢复情况。这些结果表明硝苯地平和低温的心脏保护作用是相加的。
