Hepatic dysoxia commences during O2 supply dependence.
Hepatic dysoxia commences during O2 supply dependence.
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肝脏缺氧在氧气供应依赖期间开始。
DOI：
10.1152/jappl.1992.72.4.1499
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发表时间：
1992
影响因子：
3.3
通讯作者：
E. Nemoto
中科院分区：
文献类型：
--
作者：
R. Schlichtig;H. Klions;D. Kramer;E. Nemoto
随着氧气输送（DO2）逐渐减少，肝脏的氧气消耗（VO2）保持相对恒定（与氧气供应无关），直到达到临界DO2 (DO2c)，低于该临界值，肝脏的VO2也会减少（与氧气供应相关）。这种VO2的减少是代表适应性的氧需求减少，还是组织缺氧的表现，即氧供应不足以支持氧需求，目前尚不清楚。我们通过评估6只戊巴比妥麻醉犬在氧供应独立和依赖期间进行性出血引起的肝脏线粒体NAD氧化还原状态，验证了氧供应依赖期间肝脏VO2下降代表缺氧的假设。通过测定肝静脉β -羟基丁酸与乙酰乙酸的比值（β OHB/AcAc）估计肝脏线粒体NAD氧化还原状态。DO2c值为5.02±1.64 (SD) ml.100 g-1 min-1。β -羟基丁酸与乙酰乙酸的比例恒定，直至DO2值（3.03 +/- 1.08 ml.100 g-1）。达到min-1) (P = 0.05 vs. DO2c)，然后线性增加。当DO2为5.48 +/- 2.54 ml.100 g-1时，肝脏乳酸提取率峰值为15.2 +/- 14.1%。min-1 （P = NS vs. DO2c）我们的数据支持这样的假设，即在氧气供应依赖期间VO2的减少代表组织缺氧。
Hepatic O2 consumption (VO2) remains relatively constant (O2 supply independent) as O2 delivery (DO2) progressively decreases, until a critical DO2 (DO2c) is reached below which hepatic VO2 also decreases (O2 supply dependence). Whether this decrease in VO2 represents an adaptive reduction in O2 demand or a manifestation of tissue dysoxia, i.e., O2 supply that is inadequate to support O2 demand, is unknown. We tested the hypothesis that the decrease in hepatic VO2 during O2 supply dependence represents dysoxia by evaluating hepatic mitochondrial NAD redox state during O2 supply independence and dependence induced by progressive hemorrhage in six pentobarbital-anesthetized dogs. Hepatic mitochondrial NAD redox state was estimated by measuring hepatic venous beta-hydroxybutyrate-to-acetoacetate ratio (beta OHB/AcAc). The value of DO2c was 5.02 +/- 1.64 (SD) ml.100 g-1.min-1. The beta-hydroxybutyrate-to-acetoacetate ratio was constant until a DO2 value (3.03 +/- 1.08 ml.100 g-1.min-1) was reached (P = 0.05 vs. DO2c) and then increased linearly. Peak liver lactate extraction ratio was 15.2 +/- 14.1%, occurring at a DO2 of 5.48 +/- 2.54 ml.100 g-1.min-1 (P = NS vs. DO2c). Our data support the hypothesis that the decrease in VO2 during O2 supply dependence represents tissue dysoxia.