Pichette C, Bercovici M, Goldstein M, Stinebaugh B, Tam S C, Halperin M
Crit Care Med. 1982 May;10(5):323-6. doi: 10.1097/00003246-198205000-00008.
A patient presented with lactic acidosis and severe acidemia; sodium bicarbonate was administered to titrate the very large hydrogen ion load. Coincident with this therapy, the blood lactate concentration rose from 21 to 27 mmole/L. In order to evaluate whether this rise in lactate could have occurred without requiring additional net lactic acid production, the effect of the hydrogen ion concentration on lactate distribution was evaluated. Data obtained from animal studies support the established hypothesis that lactate is distributed like other weak organic acids at steady-state; hence, alkalemia should favor a shift of lactate from the intracellular fluid (ICF) to the extracellular fluid (ECF). The authors calculated that the blood lactate concentration could rise by 50% without requiring net lactic acid accumulation when the severe acidemia was corrected by alkali therapy. Thus, an increase in lactate concentration of the magnitude observed during alkali therapy need not indicate a worsening of the metabolic picture in lactic acidosis.
一名患者出现乳酸酸中毒和严重酸血症；给予碳酸氢钠以滴定大量的氢离子负荷。在该治疗过程中，血乳酸浓度从21毫摩尔/升升至27毫摩尔/升。为了评估在不需要额外净乳酸生成的情况下乳酸浓度的这种升高是否可能发生，评估了氢离子浓度对乳酸分布的影响。从动物研究获得的数据支持已确立的假说，即乳酸在稳态时的分布与其他弱有机酸类似；因此，碱血症应有利于乳酸从细胞内液（ICF）向细胞外液（ECF）转移。作者计算得出，当通过碱疗法纠正严重酸血症时，血乳酸浓度可升高50%而无需净乳酸积累。因此，在碱疗法期间观察到的乳酸浓度升高幅度不一定表明乳酸酸中毒时代谢情况恶化。
