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

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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 hr. and a subsequent gradual decrease were observed. 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 PACO2 but that it was hardly detected during slight hyperventilation when the decrement of PACO2 was less tnan 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 m[image]/1 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 performe Animals were subjected to hyperventilation, with keeping the blood pH normal by simultaneous infusion of NH4CI, and keeping the alveolar PCO2 normal y admixing proper amounts of CO2 in the inspiratory air; 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 hypoxla, is more probably caused by a rise in intracellular pH than intracellular hypocapnla.