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急性肝衰竭时内脏对燃料底物的代谢

Splanchnic metabolism of fuel substrates in acute liver failure.

作者信息

Clemmesen J O, Høy C E, Kondrup J, Ott P

机构信息

Department of Hepatology, Rigshospitalet, University of Copenhagen, Denmark.

出版信息

J Hepatol. 2000 Dec;33(6):941-8. doi: 10.1016/s0168-8278(00)80126-9.

Abstract

BACKGROUND/AIMS: This study aimed to characterize the exchange of fuel substrates in the splanchnic circulation in acute liver failure.

METHODS

Liver vein catheterization was used in 22 patients with acute liver failure after development of hepatic encephalopathy grade III-IV Healthy controls, patients with cirrhosis and patients with acute on chronic liver disease were also studied.

RESULTS

In acute liver failure there was splanchnic removal of glucose (0.21+/-0.44 mmol/min), release of lactate (0.34+/-0.37 mmol/min), pyruvate (0.08+/-0.06 mmol/min) and ketone bodies (0.04+/-0.02 mmol/min), while extraction of amino acids and free fatty acids was insignificant. In the acute liver failure group, a normal hepatic venous oxygen saturation (0.69+/-0.12) and normal pyruvate/lactate ratio suggested absence of hypoxia even though the acetoacetate/beta-hydroxybutyrate ratio was decreased. Only in the acute liver failure group did the measured splanchnic oxygen content difference exceed what could be accounted for even by hypothesizing complete oxidation of all extracted blood-borne fuel substrates; oxidation of endogenous substrates may be quantitatively important in this condition.

CONCLUSION

Acute liver failure was associated with a state of accelerated glycolysis in the splanchnic region, leading to release of lactate in the absence of splanchnic hypoxia.

摘要

背景/目的:本研究旨在描述急性肝衰竭时内脏循环中燃料底物的交换情况。

方法

对22例发生III-IV级肝性脑病后的急性肝衰竭患者进行肝静脉插管。还研究了健康对照者、肝硬化患者和慢性肝病急性发作患者。

结果

在急性肝衰竭时,内脏摄取葡萄糖(0.21±0.44 mmol/分钟),释放乳酸(0.34±0.37 mmol/分钟)、丙酮酸(0.08±0.06 mmol/分钟)和酮体(0.04±0.02 mmol/分钟),而氨基酸和游离脂肪酸的摄取量微不足道。在急性肝衰竭组,尽管乙酰乙酸/β-羟基丁酸比值降低,但正常的肝静脉血氧饱和度(0.69±0.12)和正常的丙酮酸/乳酸比值提示不存在缺氧。仅在急性肝衰竭组,测得的内脏氧含量差值超过了即使假设所有摄取的血源性燃料底物完全氧化所能解释的范围;在这种情况下,内源性底物的氧化在数量上可能很重要。

结论

急性肝衰竭与内脏区域糖酵解加速状态有关,导致在无内脏缺氧的情况下释放乳酸。

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