Neurohr K J, Shulman R G
Adv Myocardiol. 1985;6:185-93.
Myocardial metabolism in live guinea pigs was investigated by 13C and 31P nuclear magnetic resonance (NMR) at 20.18 and 32.5 MHz, respectively. 13C NMR studies allowed monitoring of myocardial glycogen synthesis during intravenous infusion of D-[1-13C]glucose and insulin. Anoxia resulted in degradation of the labeled glycogen within 6 min and appearance of 13C label in lactic acid. Infusion of sodium [2-13C]acetate resulted in incorporation of label into the C-4, C-2, and C-3 positions of glutamate, reflecting "scrambling" of the label expected from tricarboxylic-acid-cycle activity. 31P NMR spectra of heart in live guinea pigs were obtained continuously in 20.5-sec time blocks during 3 min of anoxia, during subsequent reoxygenation, and, in separate animals, during terminal anoxia. Reversible anoxia resulted in rapid degradation of phosphocreatine (t1/2 = 54.5 +/- 2.5 sec), which recovered fully during reoxygenation. Heart inorganic phosphate increased during anoxia and returned to basal levels after oxygen was restored. During 3 min of anoxia, no significant changes in ATP levels or pH were detected.
分别在20.18兆赫和32.5兆赫下,通过13C和31P核磁共振(NMR)对活体内豚鼠的心肌代谢进行了研究。13C NMR研究能够在静脉输注D-[1-13C]葡萄糖和胰岛素期间监测心肌糖原的合成。缺氧导致标记糖原在6分钟内降解,并在乳酸中出现13C标记。输注[2-13C]醋酸钠导致标记物掺入谷氨酸的C-4、C-2和C-3位置,反映了三羧酸循环活动预期的标记物“重排”。在活体内豚鼠心脏的31P NMR光谱在缺氧3分钟期间、随后的复氧期间以及在单独的动物中在终末期缺氧期间以20.5秒的时间间隔连续获得。可逆性缺氧导致磷酸肌酸迅速降解(t1/2 = 54.5 +/- 2.5秒),在复氧期间完全恢复。心脏无机磷酸盐在缺氧期间增加,在恢复氧气后恢复到基础水平。在缺氧3分钟期间,未检测到ATP水平或pH值有显著变化。