Pyruvate in the Correction of Intracellular Acidosis: A Metabolic Basis as a Novel Superior Buffer

Fang Qiang Zhou
2005 American Journal of Nephrology  
tion, Pyrs not only correct acidosis, but also benefi t the underlying dysfunction of vital organs. In addition, Pyr is also a potential buffer component of dialysis solutions. However, the instability of Pyr in aqueous solutions restricts its clinical applications as a therapeutic agent. Attempts to create a stable Pyr preparation are needed. Since 1970s, pyruvate (Pyr) has become increasingly attractive in the protection of dysfunctional vital organs, particularly in myocardial ischemia and
more » ... perfusion injury, pointing to a potential therapeutic value for the dysfunctional myocardium [1-3] . Also, fi ndings strongly indicated that Pyr would be a novel buffer in many clinic settings [4] [5] [6] . This review discusses its distinctive effects on intracellular pH (pHi), proposing that Pyr may be superior to lactate (Lac) and bicarbonate in the correction of severe intracellular acidosis. Lactate Metabolism and Effects on pHi and Lactic Acidosis Lac has been traditionally accepted as the best replacement for bicarbonate in the treatment of metabolic acidosis since early 1930s [7] ; it has since become part of solutions for dialysis and continuous renal replacement therapy for several decades. Abstract The review focuses on biochemical metabolisms of conventional buffers and emphasizes advantages of sodium pyruvate (Pyr) in the correction of intracellular acidosis. Exogenous lactate (Lac) as an alternative of natural buffer, bicarbonate, consumes intracellular protons on an equimolar basis, regenerating bicarbonate anions in plasma while the completion of gluconeogenesis and/or oxidation occurs via tricarboxylic-acid cycle in mitochondria mainly in liver and kidney, or heart. The general assumption that Lac is 'metabolized to bicarbonate' in liver to serve as a buffer has been questioned. Pyr as a novel buffer would be superior to conventional ones in the correction of metabolic acidosis. Several likely biochemical mechanisms of Pyr action are discussed. Experimental evidence, in vivo, strongly suggested that Pyr would be particularly effi cient in the correction of severe acidemia: type A lactic acidosis, hypercapnia with cardiac arrest, and diabetic and alcoholic ketoacidosis in animal experiments and clinic settings. Because of its multi-cytoprotec-
doi:10.1159/000084141 pmid:15731550 fatcat:vbwghz5gqrgp5e2qabkn5mztoi