Woods H F, Connor H, Tucker G T
Ciba Found Symp. 1982;87:307-23. doi: 10.1002/9780470720691.ch17.
Of the two types of lactic acidosis, Type B is the most difficult to explain in terms of mechanisms of lactic acid accumulation because the tissue hypoxia that accompanies Type A is not present except as a terminal event. The methods of pharmacokinetics show that for lactate to accumulate to an extent that would disturb acid-base balance, either lactate synthesis or lactate removal would have to be increased or decreased, respectively, by about 7-10-fold. To produce lactic acidosis within a few hours, synthesis would have to increase at the same time as clearance decreased. At normal contribution of the liver to the total lactate clearance (30%-40%), a total cessation of hepatic lactate clearance would not result in lactic acidosis without a concomitant rise in the rate of lactate synthesis. Again, to produce an acidosis this increase would have to be about 8-fold at a normal fractional hepatic clearance. The control of hepatic lactate uptake is discussed in the light of the relatively low hepatic extraction of lactate and in relation to to two main models of hepatic drug (lactate) clearance; the 'well-stirred' and 'parallel-tube' models.
在两种类型的乳酸性酸中毒中，B型在乳酸积累机制方面最难解释，因为除了作为终末期事件外，A型伴随的组织缺氧并不存在。药代动力学方法表明，要使乳酸积累到会扰乱酸碱平衡的程度，乳酸合成或乳酸清除必须分别增加或减少约7至10倍。要在数小时内产生乳酸性酸中毒，合成必须在清除减少的同时增加。在肝脏对总乳酸清除的正常贡献（30%-40%）下，如果不伴随乳酸合成速率的上升，肝脏乳酸清除完全停止不会导致乳酸性酸中毒。同样，要产生酸中毒，在正常肝脏清除分数下，这种增加必须约为8倍。鉴于肝脏对乳酸的摄取相对较低，并结合肝脏药物（乳酸）清除的两种主要模型——“充分搅拌”模型和“平行管”模型，对肝脏乳酸摄取的控制进行了讨论。
