Hepatic oxygen and lactate extraction during stagnant hypoxia.
Hepatic oxygen and lactate extraction during stagnant hypoxia.
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停滞缺氧期间的肝氧和乳酸提取。
DOI：
10.1152/jappl.1991.70.1.186
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Schumacker,PT
中科院分区：
文献类型：
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作者：
Samsel,RW;Cherqui,D;Pietrabissa,A;Sanders,WM;Roncella,M;Emond,JC;Schumacker,PT
随着氧气输送量的下降，组织必须从血液中提取越来越多的氧气，以维持正常的氧气消耗量。福尔斯。在临界输送阈值以下，O2提取的增加不能补偿下降的输送，并且O2摄取福尔斯以供应依赖的方式下降。许多研究已经确定了整个动物的关键交付，但关键O2交付的区域贡献不太充分了解。在本研究中，我们探索了离体肝脏中O2提取的限制，试图确定1）肝脏中O2消耗和输送之间的正常关系，以及2）在低O2输送时肝脏乳酸提取与肝脏O2消耗下降的关系。为了回答这些问题，使用支持犬作为含氧代谢稳定血液的来源，我们研究了八个泵灌注犬肝脏。通过降低停滞缺氧模型中的血流量，我们探索了在整个生理范围内O2输送的O2消耗和输送之间的关系。临界O2输送量为28 +/- 5（SD）ml.kg-1.min-1;在达到供应依赖性之前，肝脏提取了输送O2的68 +/- 9%。这表明肝脏具有与整个身体非常相似的O2提取能力，并且与已分离的其他组织没有区别。在高血流量时，肝脏提取了血液输送的约10%的乳酸盐，但动静脉乳酸盐差异很小。然而，在低血流量时，肝脏从乳酸消耗转变为生产。与乳酸提取中的下降相一致的O2输送与临界O2输送没有显著差异。我们的结论是，减少乳酸摄取的肝脏不提前过渡到O2供应依赖。
As O2 delivery falls, tissues must extract increasing amounts of O2 from blood to maintain a normal O2 consumption. Below a critical delivery threshold, increases in O2 extraction cannot compensate for the falling delivery, and O2 uptake falls in a supply-dependent fashion. Numerous studies have identified a critical delivery in whole animals, but the regional contributions to the critical O2 delivery are less fully understood. In the present study, we explored the limits of O2 extraction in the isolated liver, seeking to determine 1) the normal relationship between O2 consumption and delivery in the liver and 2) the relationship of hepatic lactate extraction to the drop in hepatic O2 consumption at low O2 deliveries. To answer these questions, using support dogs as a source for oxygenated metabolically stable blood, we studied eight pump-perfused canine livers. By lowering the blood flow in a model of stagnant hypoxia, we explored the relationship between O2 consumption and delivery over the entire physiological range of O2 delivery. The critical O2 delivery was 28 +/- 5 (SD) ml.kg-1.min-1; the livers extracted 68 +/- 9% of the delivered O2 before reaching supply dependence. This suggests that the liver has an O2 extraction capacity quite similar to the body as a whole and not different from other tissues that have been isolated. At high blood flows, the livers extracted approximately 10% of the lactate delivered by the blood, but the arteriovenous lactate differences were small. At low blood flows, however, the livers changed from lactate consumption to production. The O2 delivery coinciding with the dropoff in lactate extraction did not differ significantly from the critical O2 delivery. We conclude that reductions in lactate uptake by the liver do not precede the transition to O2 supply dependence.