Van Dorsten F A, Nederhoff M G, Nicolay K, Van Echteld C J
Department of In Vivo NMR Spectroscopy, Bijvoet Center for Biomolecular Research, Utrecht University, NL-3584 CJ Utrecht, The Netherlands.
Am J Physiol. 1998 Oct;275(4):H1191-9. doi: 10.1152/ajpheart.1998.275.4.H1191.
Hearts of wild-type and cytosolic muscle creatine kinase (M-CK)-knockout mice were perfused with Krebs-Henseleit buffer containing 10 mM glucose and 5 mM pyruvate and studied during pacing at 400 and 600 beats/min and during K+ arrest. Phosphocreatine (PCr) and ATP concentrations in M-CK-deficient hearts were not significantly different from those in wild-type hearts. With the use of 31P NMR saturation transfer, the flux mediated predominantly by mitochondrial creatine kinase (Mi-CK) was clearly detected in M-CK-deficient hearts. Mi-CK flux was 4.8 +/- 0.6 and 4.5 +/- 0.6 mM/s during pacing at 400 and 600 beats/min, respectively, and was 3. 5 +/- 0.4 mM/s during cardiac arrest. In control hearts total CK flux was 7.8 +/- 1.1 and 6.6 +/- 1.3 mM/s during pacing at 400 and 600 beats/min, respectively, and decreased to 3.8 +/- 0.5 mM/s during arrest. It is suggested that the relative contribution of Mi-CK to the total NMR-measured CK flux in the wild-type heart is higher than that of the homodimeric M-CK isoform (MM-CK).
用含有10 mM葡萄糖和5 mM丙酮酸的Krebs-Henseleit缓冲液灌注野生型和胞质型肌肉肌酸激酶（M-CK）基因敲除小鼠的心脏，并在400和600次/分钟起搏以及钾离子停搏期间进行研究。M-CK缺陷型心脏中的磷酸肌酸（PCr）和ATP浓度与野生型心脏中的无显著差异。通过使用31P NMR饱和转移技术，在M-CK缺陷型心脏中清晰检测到主要由线粒体肌酸激酶（Mi-CK）介导的通量。在400和600次/分钟起搏期间，Mi-CK通量分别为4.8±0.6和4.5±0.6 mM/s，在心脏停搏期间为3.5±0.4 mM/s。在对照心脏中，在400和600次/分钟起搏期间，总CK通量分别为7.8±1.1和6.6±1.3 mM/s，在停搏期间降至3.8±0.5 mM/s。提示在野生型心脏中，Mi-CK对NMR测量的总CK通量的相对贡献高于同二聚体M-CK同工型（MM-CK）。
