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心肌低温保护时快速冷挛缩（rapid cooling contracture,RCC）现象近来日益受到人们重视。快速冷挛缩现象是指快速制冷诱发的非去极化的心肌挛缩。其机制可能与心肌细胞内温度依赖性Ca2+快速升高有关。降温过程中，肌浆网内存Ca2+迅速释放，并与肌钙蛋白相结合，引起蛋白构象发生变化，通过粗、细肌丝相对滑行而产生心肌收缩。快速冷挛缩的危害为能量的消耗、冠状血管阻抗增大、心脏功能降低、Ca2+超负荷等方面，尤其对于未成熟心肌危害更大。目前有些学者提出用心肌温保护和预防Ca2+超负荷等方法来避免其危害的发生。“,”The rapid cooling contracture in myocardial protection is getting more and more attention. Rapid cooling contracture is referred to as the undepolarized myocardial contracture induced by rapid cooling, which is related with the sudden increase of Ca2+. The Ca2+ released from sarcoplasmic reticulum subsequently causes myocardial contracture through the myofilaments sliding. Its deleterious effects include: more energy consumption, impaired cardiac function, Ca2+ overload, et al. And some investigators have put forward some principals to prevent the bad influences of rapid cooling contracture.