BLOOD LACTATE ACCUMULATION AND ITS CAUSATIVE FACTORS DURING PASSIVE HYPERVENTILATION IN DOGS

Abstract

Accumulation of lactate in blood during passive hyperventilation and the causative factors for this phenomenon were investigated in anesthetized dogs. In severe, sustained hyperventilation, a striking increase in blood lactate within 2 hours and a subsequent gradual decrease were observed. Furthermore, it was manifested from an experiment in which the ventilation was progressively raised that the increase in lactate was proportionally related to the decrease in P_Aco₂ but that it was hardly detected during slight hyperventilation when the decrement of P_Aco₂ was less than 15 mmHg. The plasma bicarbonate under the standard conditions (SCB) proposed by PETERS and VAN SLYKE was calculated in the same experimental group and approximately 42% of its decrement up to 7 mM/l was found to be accounted for by the increased blood lactate.
For the purpose of exploring the factor controlling the lactic acid production of tissue cells in the acid-base disturbance such as seen in hyperventilation, a series of experiments were performed: 1) Animals were subjected to hyperventilation, with a) keeping the blood pH normal by simultaneous infusion of NH₄Cl, and b) keeping the alveolar Pco₂ normal by admixing proper amounts of CO₂ in the inspiratory air. 2) Immobilized animals were infused intravenously with NaHCO₃ or THAM solutions, alveolar Pco₂ being maintained at a normal level by artificially controlling the ventilation rate. By examining the time course of blood lactate in these animals, it was deduced that the increase in blood lactate, in the acid-base disturbance including hyperventilatory alkalemia unaccompanied by tissue hypoxia, is more probably caused by a rise in intracellular pH than intracellular hypocapnia.