Sodium bicarbonate has been established for long time as the first choice on the treatment of metabolic acidosis. Meanwhile, Cohen and Woods classified lactic acidosis which plays a major role of metabolic acidosis into type A, accompanied by hypoxia, and type B₁, B₂ & B₃, without hypoxia. It has been well known that sodium bicarbonate aggravate type B group lactic acidosis. Recently, Arieff and others insisted that the onset of type B was initiated by hypotension with hypoxia. Graf and others verified type A always accompanied with type Bs.
Sodium bicarbonate does alkalize extracellularly only and increase hydogen content intracellulary by diffusion of carbon dioxide into cells.
Hyperosmolarity induced by its administration caused release of hydrogen from erythrocytes as well as decreased P₅₀ value.
Hepatic cellular acidosis followed by sodium bicarbonate administration gave rise to lactate acidosis in vicious cycle.
It should be notified that sodium l-lactate should never cause elevation of lactate levels in blood. There is competitive uptake by cellular menbrane between d-lactate and l-type.
On racemic sodium lactate in Hartmann's solution, however, 30% of d-sodium lactate will be not metabolized to bicarbonate.
Graf suggested use of dichloroaccetate for type A lactic acidosis, while author's experiment on its use was unsatisfied.
Use of THAM could be reconsidered, however, its disadvantages has been reported by many.
Redox potentials in the cytosol could be improved by either use of THAM or DCA as well as methylene blue, but they were not good for redox state in the mitochondria. Author afraid of over-production of β OH-butylate from acetoacetate by their use in mitochondria.
So far, besides a grave of branched chain aminoacids, sodium bicarbonate has still superiority on any alkalizing agents. As Ryder notified, low dose long time infusion of sodium bicarbonate aimed to attain the minimum levels of arterial PH 7.20 and 10mE/L of HCO₃ content, should be recommeneded.
On the same time, lactate clearance by the liver should be supported by increased portal blood flow by infusion of dopamin as well as enriched oxygen delivery.