Pathophysiology of type A hypoxic lactic acidosis in dogs

Abstract

Hypoxic lactic acidosis (HLA) was induced in dogs by ventilating them with a hypoxic gas mixture of 8% O2-92% N2. The animals were studied both in the control state and after development of HLA, where arterial lactate was above 5 mM, pH was below 7.2, bicarbonate was below 12 mM, and arterial PO2 was between 26 and 30 Torr. After hypoxia had been present for 90 min, most of the increase in arterial lactate vs. control was due to increased lactate production from gut and carcass in the presence of a decreased capacity of the liver to extract lactate. The capacity of the liver to extract lactate in the normoxic state was evaluated in another group of six dogs after infusion of L-lactic acid such that arterial pH, lactate, and bicarbonate were similar to hypoxic values. In these experiments it was found that the capacity of the liver to extract lactate was 14.8 +/- 1.7% of the delivered load vs. 4.9 +/- 1.3% observed in hypoxic animals. The decreased liver lactate extraction in HLA was probably secondary to both a decrease in liver oxygen uptake and a decrease in liver intracellular pH and was paralleled by an increase in liver tissue lactate levels. Cardiac output, in contrast to other forms of lactic acidosis, was increased by 40% vs. control and femoral artery flow by 35%, whereas liver blood flow was unchanged and renal blood flow decreased. Hypoxic lactic acidosis thus is the consequence of overproduction of lactate by both gut and carcass, in the presence of impaired utilization of lactate by the liver.(ABSTRACT TRUNCATED AT 250 WORDS)