Pathophysiology and Experimental Tomography Center, Aarhus Hospital, Aarhus University Hospitals, Aarhus, Denmark.
Metab Brain Dis. 2010 Mar;25(1):57-63. doi: 10.1007/s11011-010-9179-9. Epub 2010 Feb 25.
Hepatic encephalopathy is a condition of reduced brain functioning in which both blood flow and brain energy metabolism declined. It is not known whether blood flow or metabolism is the primary limiting factor of brain function in this condition. We used calculations of mitochondrial oxygen tension to choose between cause and effect in three groups of volunteers, including healthy control subjects (HC), patients with cirrhosis of the liver without hepatic encephalopathy (CL), and patients with cirrhosis with acute hepatic encephalopathy. Compared to HC subjects, blood flow and energy metabolism had declined in all gray matter regions of the brain in patients with HE but not significantly in patients with CL. Analysis of flow-metabolism coupling indicated that blood flow declined in HE as a consequence of reduced brain energy metabolism implied by the calculation of increased mitochondrial oxygen tensions that patients with HE were unable to utilize. We ascribe the inability to use the delivered oxygen of patients with HE to a specific inhibition associated with oxidative metabolism in mitochondria.
肝性脑病是一种脑功能降低的病症，其特点是血流量和脑能量代谢下降。目前尚不清楚在这种情况下，是血流量还是代谢是脑功能的主要限制因素。我们使用线粒体氧张力的计算来在三组志愿者中选择因果关系，包括健康对照组（HC）、无肝性脑病的肝硬化患者（CL）和急性肝性脑病的肝硬化患者。与 HC 受试者相比，HE 患者的大脑所有灰质区域的血流量和能量代谢都下降了，但 CL 患者的血流量和能量代谢并没有显著下降。对血流-代谢偶联的分析表明，HE 患者的脑血流量下降是由于脑能量代谢减少所致，这是通过计算线粒体氧张力增加得出的，表明 HE 患者无法利用。我们将 HE 患者无法利用输送的氧气归因于与线粒体氧化代谢相关的特定抑制。
