Kaufman I A, Hall N F, DeLuca M A, Ingwall J S, Mayer S E
Am J Physiol. 1977 Aug;233(2):H282-8. doi: 10.1152/ajpheart.1977.233.2.H282.
Intact beating fetal mouse hearts in organ culture were deprived of oxygen and glucose for up to 4 h, resulting in loss of beating, an 80% fall in ATP, reduction of energy charge from 0.85 to 0.48, and doubling of total nucleoside concentration. Radiolabeled adenine nucleotides were degraded to hypoxanthine and inosine, which were lost from the hearts into the medium during the deprivation period. Adenosine and adenine also appeared in the medium when adenosine deaminase was inhibited. After 24 h of O2 and glucose resupply, ATP returned to 60% of control, and energy charge rose to 0.76. Labeled nucleosides and bases remaining in the heart or exogenous labeled adenine were utilized to resynthesize ATP. [14C]glycine was rapidly taken up by recovering hearts but was not used for de novo adenine nucleotide synthesis. Ability to recover ATP and spontaneous contraction appear related to residual nucleotide and nucleoside content rather than to energy charge.
将处于器官培养中的完整搏动的胎鼠心脏缺氧缺糖长达4小时，导致心脏停止搏动，ATP含量下降80%，能荷从0.85降至0.48，总核苷浓度翻倍。放射性标记的腺嘌呤核苷酸降解为次黄嘌呤和肌苷，在缺氧缺糖期间从心脏进入培养基。当腺苷脱氨酶被抑制时，腺苷和腺嘌呤也出现在培养基中。在重新供应氧气和葡萄糖24小时后，ATP恢复到对照值的60%，能荷升至0.76。心脏中剩余的标记核苷和碱基或外源性标记腺嘌呤被用于重新合成ATP。[14C]甘氨酸被恢复中的心脏迅速摄取，但未用于从头合成腺嘌呤核苷酸。恢复ATP的能力和自发收缩似乎与残余核苷酸和核苷含量有关，而不是与能荷有关。
