Bristow J, Rudolph A M, Itskovitz J, Barnes R
J Clin Invest. 1983 May;71(5):1047-61. doi: 10.1172/jci110855.
Although the fetal liver is an active metabolic organ, its oxygen and glucose requirements have not previously been described. We measured hepatic blood flows and the oxygen and glucose differences across the liver in 12 late gestation fetal lambs in utero. Four animals were studied at least 1 wk postsurgically and again 2-5 d later to assess daily variations in hepatic blood flow and metabolism (group I). A second group of eight animals was studied 3-5 d postsurgically during a control period and during acute fetal hypoxia (group II). Under control conditions total hepatic blood flow averaged 400 ml/min per 100 g in both groups, and 75-80% was of umbilical origin. Liver blood flow and oxygen consumption were usually similar during repeated measurements, but in one animal varied considerably. During periods of normoxia, oxygen consumption for both the right and left lobes of liver was 4 ml/min per 100 g. Oxygen consumption of the whole liver accounted for 20% of total fetal oxygen consumption. This was achieved with oxygen extraction of 10-15%, so that hepatic venous blood was well oxygenated and provided an important source of oxygen for other fetal tissues. Under control conditions we could demonstrate no net hepatic uptake or release of glucose suggesting that the liver ultimately utilizes another carbon source to support its oxidative metabolism. During acute hypoxia total liver blood flow and its umbilical venous contribution both fell by 20%. Blood flow to the right lobe of the liver fell twice as much as that to the left lobe. Hepatic oxygen consumption was linearly related to oxygen delivery during the control and hypoxic periods. Consequently, right hepatic oxygen uptake fell by 45% whereas left hepatic oxygen uptake was unchanged, suggesting a functional difference between the lobes. During hypoxia glucose was released from both liver lobes; 6 mg/min per 100 g for the right lobe and 9 mg/min per 100 g for the left lobe. Total hepatic release of glucose was estimated to nearly equal umbilical uptake, so that 45% of the glucose available to fetal tissues was of hepatic origin. We conclude that the fetal liver responds to acute hypoxia by reducing its own oxygen consumption and releasing glucose to facilitate anaerobic metabolism.
尽管胎儿肝脏是一个活跃的代谢器官，但其氧和葡萄糖需求此前尚未被描述。我们测量了12只妊娠晚期子宫内胎羊的肝脏血流以及肝脏两侧的氧和葡萄糖差值。4只动物在术后至少1周进行研究，并在2 - 5天后再次研究，以评估肝脏血流和代谢的每日变化（第一组）。第二组8只动物在术后3 - 5天的对照期和急性胎儿缺氧期间进行研究（第二组）。在对照条件下，两组每100克肝脏的总血流平均为400毫升/分钟，且75 - 80%来自脐血。在重复测量期间，肝脏血流和氧消耗通常相似，但有一只动物变化很大。在常氧期，肝脏左右叶的氧消耗均为每100克4毫升/分钟。整个肝脏的氧消耗占胎儿总氧消耗的20%。这是通过10 - 15%的氧摄取实现的，因此肝静脉血氧合良好，为其他胎儿组织提供了重要的氧源。在对照条件下，我们未发现肝脏有葡萄糖的净摄取或释放，这表明肝脏最终利用另一种碳源来支持其氧化代谢。在急性缺氧期间，肝脏总血流及其脐静脉供血均下降了20%。肝脏右叶的血流下降幅度是左叶的两倍。在对照期和缺氧期，肝脏氧消耗与氧输送呈线性相关。因此，肝脏右叶的氧摄取下降了45%，而左叶的氧摄取未变，这表明两叶之间存在功能差异。在缺氧期间，肝脏两叶均释放葡萄糖；右叶为每100克6毫克/分钟，左叶为每100克9毫克/分钟。肝脏葡萄糖总释放量估计几乎等于脐血摄取量，因此胎儿组织可用葡萄糖的45%来自肝脏。我们得出结论，胎儿肝脏通过降低自身氧消耗和释放葡萄糖来促进无氧代谢，从而对急性缺氧作出反应。
