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循环性肝抑制因子降低肝切除术后残余肝脏的能量电荷水平。

Circulating hepatodepressant factors decreasing the energy charge levels of the remnant liver after hepatectomy.

作者信息

Ozawa K, Yamaoka Y, Kimura K, Kamiyama Y, Sato M, Ukikusa M, Tobe T

出版信息

Eur Surg Res. 1981;13(6):444-57. doi: 10.1159/000128213.

Abstract

In 25% hepatectomized rabbits, the mitochondrial phosphorylative activity and the energy charge [(ATP + 1/2 ADP)/(ATP + ADP + AMP)] levels of the remnant liver remained unchanged after hepatectomy. In 70% hepatectomized rabbits, the energy charge levels of the remnant liver decreased maximally 24 h after hepatectomy (p less than 0.001), simultaneously with a marked enhancement of mitochondrial phosphorylative activity (P less than 0.001). Afterward, both returned to normal levels within 4 days. In 93% hepatectomized rabbits, the energy charge levels fell rapidly, with an inhibition of mitochondrial phosphorylative activity, within 6 h after hepatectomy. When a 24-hour 70% hepatectomized rabbit was cross-circulated with a normal rabbit, the energy charge in the liver of the normal partner decreased to 0.732 at 30 min after the blood exchange and then returned to 0.855 while that in the remnant liver of the hepatectomized partner increased from 0.767 to 0.820 (p less than 0.001). Also, the energy charge values of a 24-hour 70% hepatectomized rabbit were increased by the extracorporeal normal liver perfusion. It is suggested that a decrease in the energy charge of the remnant liver is due, at least partly, to the accumulation of the substances consuming hepatic energy (hepatodepressant factors) in the systemic blood of hepatectomized rabbits.

摘要

在切除25%肝脏的兔子中,肝切除术后残余肝脏的线粒体磷酸化活性和能荷水平[(ATP + 1/2 ADP)/(ATP + ADP + AMP)]保持不变。在切除70%肝脏的兔子中,残余肝脏的能荷水平在肝切除术后24小时降至最低(p < 0.001),同时线粒体磷酸化活性显著增强(P < 0.001)。此后,两者在4天内恢复到正常水平。在切除93%肝脏的兔子中,能荷水平在肝切除术后6小时内迅速下降,同时线粒体磷酸化活性受到抑制。当一只切除70%肝脏24小时的兔子与一只正常兔子进行交叉循环时,正常兔子肝脏的能荷在血液交换后30分钟降至0.732,然后恢复到0.855,而切除肝脏兔子的残余肝脏能荷从从0.767增加到0.820(p < 0.001)。此外,对一只切除70%肝脏24小时的兔子进行体外正常肝脏灌注可提高其能荷值。提示残余肝脏能荷降低至少部分归因于肝切除兔子全身血液中消耗肝脏能量的物质(肝脏抑制因子)的积累。

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