Energy metabolism following prolonged hepatic cold preservation: Benefits of interrupted hypoxia on the adenine nucleotide pool in rat liver
Energy metabolism following prolonged hepatic cold preservation: Benefits of interrupted hypoxia on the adenine nucleotide pool in rat liver
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DOI：
10.1006/cryo.1999.2191
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发表时间：
1999-09-01
期刊：
影响因子：
2.7
通讯作者：
Fuller, BJ
中科院分区：
文献类型：
--
作者：
Mitchell, SJ;Churchill, TA;Fuller, BJ
在离体大鼠肝脏保存 5、10 和 24 小时后，研究了短暂低温再灌注 (HtR) 在冷缺氧保存期后恢复肝脏能量代谢的能力。此外，还研究了 HtR 在长时间（24 小时）缺氧保存期间恢复肝脏氧化代谢的效果。所有组均使用组氨酸-乳糖酸-棉子糖溶液进行初始冷门静脉冲洗。结果表明，冷缺氧 5 或 10 小时可使肝脏能够实现相似的 ATP、能量电荷和总腺嘌呤核苷酸恢复，但 24 小时冷保存后的 HtR 导致 ATP 再生减少、能量电荷降低和组织腺嘌呤核苷酸下降。当肝脏静止 24 小时，但在 5 或 10 小时后返回缺氧储存之前进行短暂的 HtR 时，能量代谢物的回收率比单独缺氧 24 小时后记录的回收率有所提高。事实上，这些改善并非由于腺嘌呤核苷酸前体供应的改善所致，这一事实已通过研究组得到证实，这些研究组在 24 小时冷缺氧后给予含有腺嘌呤核苷酸前体（腺苷、腺嘌呤和肌苷）的灌注液的 HtR。这些数据与以下假设一致：长期肝脏冷藏后代谢恢复不良更多是由于线粒体氧化磷酸化减少而不是腺嘌呤核苷酸再合成前体缺乏所致。此外，在低温条件下短暂恢复氧化代谢可以在一定程度上保护长期储存后的最终代谢状态。 (C) 1999 年学术出版社。
The ability of brief hypothermic reperfusion (HtR) to restore hepatic energy metabolism following periods of cold hypoxic preservation was studied in isolated rat livers after storage times of 5, 10, and 24 h. In addition, investigations were performed on the effects of HtR used to restore Liver oxidative metabolism in the middle of a prolonged (24 h) hypoxic preservation period. A histidine-lactobionate-raffinose solution was used for the initial cold portal flush in all groups. Results showed that cold hypoxia for either 5 or 10 h yielded livers capable of similar recoveries of ATP, energy charge, and total adenine nucleotides, but that HtR after 24 h cold preservation resulted in reduced regeneration of ATP, a lower energy charge, and a fall in tissue adenine nucleotides. When Livers were stead for 24 h but subjected to brief HtR after either 5 or 10 h before return to hypoxic storage, improved recoveries of the energy metabolites were seen over those recorded after 24 h hypoxia alone. The fact that these improvements were not due to an improved supply of adenine nucleotide precursors was demonstrated by studying groups which were given HtR with perfusate containing precursors of adenine nucleotides (adenosine, adenine, and inosine) after 24 h cold hypoxia. These data are consistent with the hypothesis that poor metabolic recovery after long-term hepatic cold preservation results more from decreased mitochondrial oxidative phosphorylation than from a lack of precursors for adenine nucleotide resynthesis. In addition, restoring oxidative metabolism at hypothermia for brief periods can to some extent protect final metabolic status after prolonged storage. (C) 1999 Academic Press.