Adenosine triphosphate compartmentation in living hearts: a phosphorus nuclear magnetic resonance saturation transfer study.
Adenosine triphosphate compartmentation in living hearts: a phosphorus nuclear magnetic resonance saturation transfer study.
复制标题
活体心脏中的三磷酸腺苷区室：磷核磁共振饱和转移研究。
作者：
R. Nunnally;D. Hollis
本文报道了用饱和转移技术对肌酸磷酸激酶（CPK）动力学的~（31）P核磁共振（NMR）研究。灌注心脏中的磷酸肌酸（PCr）和三磷酸腺苷（ATP）水平可以通过实验改变，方法是停止灌注（缺血）至心脏35分钟，然后再灌注以产生稳定的性能水平。通过在灌注液中给予25 mM氯化钾（KCl）来改变心脏对能量的利用，从而阻止心肌收缩。与对照心脏研究相比，在缺血和KCl停搏期间测量的单向速率改变。在对照实验中观察到的速率表明CPK系统不处于稳定状态。这种明显偏离稳态条件是由于ATP的细胞内区室化的存在。
31P nuclear magnetic resonance (NMR) studies of creatine phosphokinase (CPK) kinetics using saturation transfer techniques are reported. The phosphocreatine (PCr) and adenosine triphosphate (ATP) levels in perfused hearts can be altered experimentally by stopping the flow of perusate (ischemia) to the heart for 35-min periods, followed by reperfusion to produce stable levels of performance. Utilization of energy by the heart was altered by administration of 25 mM potassium chloride (KCl) in the perfusate, which arrests contraction of the myocardium. Compared with control heart studies, the unidirectional rates measured during ischemia and KCl arrest are altered. The rates observed in the control experiments indicate that the CPK system is not in a steady state. This apparent deviation from steady-state conditions is ascribed to the existence of intracellular compartmentation of ATP.