Yan L N, Ozawa K, Kobayashi N
Department of Surgery, First Hospital, West China University of Medical Sciences, Chengdu.
Chin Med J (Engl). 1992 Aug;105(8):684-8.
The changes in the cellular concentrations of ATP, ADP, AMP and oxidative phosphorylation of mitochondria in the liver were investigated experimentally in rats with acute pancreatitis (AP). The energy charge (ATP + 1/2ADP)/(ATP+ ADP+ AMP) of the liver decreased from 0.866 to 0.806 (P < 0.05) at 24 hours after onset of AP, and continuously decreased to 0.769 (P < 0.01) at 48 hours. On the other hand, the mitochondrial phosphorylative activity increased rapidly to 130% and 157% in the controls at 12 hours and 24 hours respectively and then decreased rapidly at 48 hours. The blood ketone body ratios were paralleled to the hepatic energy charge level in AP rats. These findings suggest that the nature of the derangement of the hepatic energy metabolism initiated by AP is that the effects of mitochondria damage result in a significant decrease in liver energy charge level, leading ultimately to hepatocellular impairment, and the measurement of the blood ketone body ratio is useful in evaluating the energy status of the liver in AP patients.
通过实验研究了急性胰腺炎（AP）大鼠肝脏中ATP、ADP、AMP的细胞浓度变化以及线粒体的氧化磷酸化情况。AP发病后24小时，肝脏的能荷（ATP + 1/2ADP）/（ATP + ADP + AMP）从0.866降至0.806（P < 0.05），并在48小时持续降至0.769（P < 0.01）。另一方面，对照组中线粒体磷酸化活性在12小时和24小时分别迅速升至130%和157%，然后在48小时迅速下降。AP大鼠的血酮体比值与肝脏能荷水平平行。这些发现表明，AP引发的肝脏能量代谢紊乱的本质是线粒体损伤导致肝脏能荷水平显著降低，最终导致肝细胞损伤，并且血酮体比值的测定有助于评估AP患者肝脏的能量状态。
