Bowditch J, Brown A K, Dow J W
Biochim Biophys Acta. 1985 Feb 21;844(2):119-28. doi: 10.1016/0167-4889(85)90082-5.
Reoxygenation of ischaemic, energy-depleted heart does not result in sufficiently rapid regeneration of normal adenine nucleotide concentrations for preservation of cardiac function and structure. Salvage of nucleoside as a mechanism for restoration of ATP in the post-ischaemic myocardium is limited by efflux of adenosine during ischaemia. Isolated cardiac myocytes have been used to establish the kinetics of uptake and salvage of adenosine and inosine, measuring the distribution of radioactive nucleoside incorporated into ATP, ADP and AMP. Maximum rates of catalysis of reactions on the salvage pathway, and of enzymes competing for substrates on the pathway, have been established in myocyte extracts. Myocytes have little capacity to salvage or catabolise inosine. Enzyme measurements indicate that salvage of adenosine should proceed at 7-8-times the rate exhibited by intact myocytes dependent upon extracellular adenosine as substrate. The data indicate that the rate of transport of adenosine is not determined by its metabolic utilization, but is the rate-limiting step in the salvage of adenosine.
缺血、能量耗竭的心脏再灌注时，正常腺嘌呤核苷酸浓度的再生速度不够快，无法维持心脏功能和结构。核苷补救作为缺血后心肌中ATP恢复的一种机制，受到缺血期间腺苷外流的限制。分离的心肌细胞已被用于确定腺苷和肌苷摄取及补救的动力学，测量掺入ATP、ADP和AMP中的放射性核苷的分布。在心肌细胞提取物中已确定了补救途径上反应的最大催化速率以及与该途径上底物竞争的酶的最大催化速率。心肌细胞挽救或分解代谢肌苷的能力很小。酶的测定表明，依赖细胞外腺苷作为底物时，腺苷补救的速率应是完整心肌细胞所显示速率的7-8倍。数据表明，腺苷的转运速率不是由其代谢利用决定的，而是腺苷补救中的限速步骤。
