论文部分内容阅读
心肌对缺血非常敏感,冠状动脉血流被阻断仅1分钟,缺血心肌的收缩功能即迅速丧失,而且这一局部功能性损害可持续数小时甚至数天。缺血后心肌功能性恢复的障碍是由于ATP、GTP、CTP等各种瞟呤核苷酸不能得到及时的补充所引起的。国外一些学者研究了一种嘌呤前身5-氨基咪唑-4-甲酰胺核苷(5-amino-imidazole-4-carboxamide riboside,简写为AICAriboside)在正常心肌的代谢途径,并发现它对缺血后心肌的修复过程有促进作用。
Myocardium is very sensitive to ischemia, coronary blood flow is blocked for only 1 minute, and the contractile function of ischemic myocardium is rapidly lost, and this local functional impairment can last for hours or even days. Myocardial dysfunction after myocardial ischemia recovery is due to ATP, GTP, CTP and other various purine nucleotides can not be promptly replenished caused. Some foreign scholars have studied a purine precursor 5-amino-imidazole-4-carboxamide riboside (AICAriboside) metabolic pathway in normal myocardium and found it after ischemia Myocardial repair process has a catalytic effect.