Nishida T, Koseki M, Kamiike W, Nakahara M, Nakao K, Kawashima Y, Hashimoto T, Tagawa K
Transplantation. 1987 Jul;44(1):16-21. doi: 10.1097/00007890-198707000-00005.
Biochemical markers of ischemic injury of rat liver were studied in an extracorporeal perfusion system. During anoxic perfusion, purine compounds appeared in the perfusate as soon as they were formed in the liver and their recovery in the perfusate balanced the loss of adenine nucleotides from the liver. In contrast, cytosolic aspartate aminotransferase did not appear in the perfusate at slow rates of liver perfusion or during hypothermic perfusion. The production of purine compounds was further investigated in hypothermically preserved liver in connection with the restoration of some metabolic functions of liver. The amount of purine compounds released into the perfusate was found to be closely related to the degrees of damage of the hepatic functions of gluconeogenesis, ureogenesis, and mitochondrial respiration on reperfusion. These results indicate that release of purine compounds into the perfusate is a good marker of ischemic damage.
在体外灌注系统中研究了大鼠肝脏缺血损伤的生化标志物。在缺氧灌注期间,嘌呤化合物在肝脏中一形成就出现在灌注液中,并且它们在灌注液中的回收平衡了肝脏中腺嘌呤核苷酸的损失。相比之下,在肝脏灌注速率缓慢或低温灌注期间,胞质天冬氨酸转氨酶并未出现在灌注液中。结合肝脏某些代谢功能的恢复,对低温保存的肝脏中嘌呤化合物的产生进行了进一步研究。发现释放到灌注液中的嘌呤化合物的量与再灌注时糖异生、尿素生成和线粒体呼吸等肝功能损伤程度密切相关。这些结果表明,嘌呤化合物释放到灌注液中是缺血损伤的一个良好标志物。