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未成熟心肌的组织结构与代谢特征不同于成熟心肌.要儿开心术前往往处在缺氧容量压力负荷增高的应急状态,因此对心肌保护提出了特殊要求。本文通过文献复习对未成熟心肌保护技术的基础理论及其临床应用的进展作一综述。 一、未成熟心肌的生理代谢特点低温能延长未成熟心肌缺血的安全时间,其对保护较高ATP水平及迅速停跳的作用是十分明显的。未成熟心肌比成熟心肌更耐缺血的原因是它的早期依赖于无氧酵解,另外一个原因是未成熟心肌5一核苷酸酶5’～nucleotidase)含量较低。这保证了缺血期间维持较高的ATP前体水平~[1]。同时未成熟心肌可通过氨基转移来获能亦是未成熟心肌细胞代谢的一大特征~[2]。低温对未成熟心肌也有不利的一面,Rebeyka等~[3]观察到低温能引起停跳前未成熟心肌挛缩而造成类似心肌缺血性损害。其机制可能与钙向细胞内流有关~[4]。冷挛缩现象的认识可能对常规深低温体外技术提出新课题。
Immature myocardial tissue structure and metabolic characteristics are different from mature myocardium. To children happy preoperative often in the hypoxic capacity of the stress load increased emergency, so myocardial protection made special requirements. This review summarizes the basic theory of immature myocardial protection and its clinical application through literature review. First, the physiological characteristics of immature myocardial hypothermia can extend the immature myocardial ischemia safe time, its role in the protection of high ATP levels and rapid arrest is very obvious. Immature myocardium is more resistant to ischemia than mature myocardium due to its early reliance on anaerobic glycolysis, another reason is the immature myocardial 5-nucleotidase 5 ’- nucleotidase) content is low. This ensures that a high ATP precursor level is maintained during ischemia [1]. At the same time, immature myocardium can be acquired through the amino transfer is also a major feature of immature cardiomyocyte metabolism ~ [2]. Low temperature on the immature myocardium also has a negative side, Rebeyka et al [3] observed that hypothermia can cause premature beating unmyelinated contracture caused by similar myocardial ischemic damage. The mechanism may be related to the influx of calcium to the cells ~ [4]. Recognition of the phenomenon of cold contracture may pose a new topic for conventional deep cryogenic in vitro techniques.