Reimer K A, Jennings R B
Acta Med Scand Suppl. 1981;651:19-27. doi: 10.1111/j.0954-6820.1981.tb03628.x.
In summary, myocardial ischemia is associated with the progressive depletion of HEP and the adenine nucleotide pool. Anaerobic glycolysis is essential for energy production in the severely ischemic myocyte and accounts for 80% of the HEP utilized by severely or totally ischemic myocardium. However, the rate of anaerobic glycolysis is too slow to prevent the progressive depletion of ATP. Anaerobic glycolysis stops entirely prior to the complete utilization of glycogen. Without remaining HEP stores or HEP production from anaerobic glycolysis, HEP utilization no longer can occur. This point occurs in vivo after about 40 minutes of severe ischemia and coincides with the onset of cell death. Modest depletion of ATP due to brief periods of transient ischemia may not cause cell death, but is associated with partial depletion of the adenine nucleotide pool. The slow repletion of this pool may be responsible for prolonged depression of contractile function.
总之,心肌缺血与高能磷酸化合物(HEP)和腺嘌呤核苷酸池的逐渐耗竭相关。无氧糖酵解对于严重缺血心肌细胞的能量产生至关重要,且占严重或完全缺血心肌所利用的HEP的80%。然而,无氧糖酵解的速率过慢,无法阻止ATP的逐渐耗竭。在糖原完全耗尽之前,无氧糖酵解就会完全停止。没有剩余的HEP储备或无氧糖酵解产生的HEP,就无法再进行HEP的利用。这一情况在体内严重缺血约40分钟后发生,与细胞死亡的开始相吻合。短暂的短暂性缺血导致的ATP适度耗竭可能不会导致细胞死亡,但与腺嘌呤核苷酸池的部分耗竭有关。该池的缓慢补充可能是收缩功能长期抑制的原因。