Dow J W, Nigdikar S, Bowditch J
Biochim Biophys Acta. 1985 Nov 20;847(2):223-7. doi: 10.1016/0167-4889(85)90024-2.
Inadequate oxygenation of cardiac muscle leads to rapid loss of high energy compounds essential for contractile function. ATP can be regenerated by synthesis de novo, a route operating at a relatively slow rate in the heart. Myocytes isolated from mature rat heart have been used to measure the rate of ATP synthesis de novo from both [14C]glycine and [14C]ribose. Incorporation of glycine into ATP is accelerated 10-fold in the presence of 1 mM ribose. Myocytes also accumulate both precursors into IMP and four other metabolites on the de novo synthesis pathway. These metabolites represent 80% of the glycine entering the pathway. The potential of de novo synthesis for restoration of adenine nucleotides appears to be limited by the rates of early reactions, adenylosuccinate synthetase being only one of the enzymes operating at a sufficiently slow rate to make this pathway an inherently weak route for the restoration of normal energy status in post-ischemic myocardium. Interventions are being sought to alleviate these apparent metabolic delays.
心肌氧合不足会导致对收缩功能至关重要的高能化合物迅速流失。ATP可通过从头合成再生，这一途径在心脏中以相对较慢的速度运作。从成年大鼠心脏分离出的心肌细胞已被用于测量从[14C]甘氨酸和[14C]核糖从头合成ATP的速率。在1 mM核糖存在的情况下，甘氨酸掺入ATP的速度加快了10倍。心肌细胞还会将两种前体物质积累到肌苷一磷酸（IMP）以及从头合成途径上的其他四种代谢产物中。这些代谢产物占进入该途径的甘氨酸的80%。从头合成恢复腺嘌呤核苷酸的潜力似乎受到早期反应速率的限制，腺苷酸琥珀酸合成酶只是以足够慢的速率运作的酶之一，这使得该途径成为缺血后心肌恢复正常能量状态的固有弱途径。目前正在寻求干预措施来缓解这些明显的代谢延迟。
