Intravenous acid infusion without lowering arterial pH stimulates breathing

The aim of this study was to determine whether increases in ventilation would occur during intravenous acid infusion even if systemic arterial pH was held constant. In six awake ponies, HCl (500 ml, approximately 0.312 M) was infused into the right atrium at a total dose of 1.0 meq/kg over 18 min wh...

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Published inJournal of applied physiology (1985) Vol. 60; no. 3; p. 861
Main Authors Orr, J A, Erichsen, D F, Shirer, H W, Allen, P L, Payne, P A
Format Journal Article
LanguageEnglish
Published United States 01.03.1986
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Summary:The aim of this study was to determine whether increases in ventilation would occur during intravenous acid infusion even if systemic arterial pH was held constant. In six awake ponies, HCl (500 ml, approximately 0.312 M) was infused into the right atrium at a total dose of 1.0 meq/kg over 18 min while an equivalent dose of NaOH was infused into the left heart to restore systemic arterial pH to normal. Total ventilation increased at the onset of the infusion and remained elevated although systemic arterial pH was normal to slightly alkaline. The increase in ventilation during the initial 2 min of the infusion coincided with an increase in pulmonary arterial PCO2 and decrease in pulmonary arterial pH. As the infusion progressed, however, pulmonary arterial pH and PCO2 returned to near control values due to the recirculation of systemic arterial blood with an acid-base status that had been altered consequent to the hyperventilation. Pulmonary arterial blood pressure was increased significantly during the entire infusion. Infusion of equivalent doses of hypertonic saline led to only minor alterations in the variables that were measured. These experiments demonstrate that this dose of intravenous HCl can increase ventilation independent of reductions in systemic arterial pH. Because increases in ventilation and pulmonary arterial H+ were not well correlated throughout the entire infusion, and pulmonary arterial blood pressure was increased, it is not clear if the mechanism for this ventilatory response is due to stimulation of pulmonary chemoreceptors, pulmonary vascular mechanoreceptors, or some other mechanism unrelated to increases in systemic arterial H+ concentration.
ISSN:8750-7587
DOI:10.1152/jappl.1986.60.3.861