Ventilatory responses to transient acidic and hypercapnic vertebral artery infusions

Robert S. Fitzgerald, Nicholas Gross, Robert E. Dutton

Research output: Contribution to journalArticle

Abstract

Transient infusions of normal, acidic, hypercapnic, or buffered hypercapnic blood were made into the vertebral arteries of anesthetized dogs. The infusions of normal or acidic (hyperhydric-isocapnic) blood produced no statistical changes in ventilation during a 100 second infusion period. The infusions of hypercapnic blood produced an increase in ventilation after a delay of 20-30 sec, while the infusions of equally hypercapnic blood buffered with HCO-3, which prevented the normal drop in pH, produced a greater and more prompt increase in ventilation. These results suggest that under physiological conditions: 1) increased acidity of arterial blood does not stimulate the central chemoreceptors in the absence of an increase in PCO2; 2) the blood-borne agent leading to stimulation of the central chemoreceptors is molecular CO2; 3) increased blood [Hco-3] initially facilitates the stimulation of the centra] chemoreceptors during hypercapnia; 4) a sudden transitory change in arterial Pco produces its initial effect upon ventilation by stimulating chemoreceptors at the periphery.

Original languageEnglish (US)
Pages (from-to)387-395
Number of pages9
JournalRespiration Physiology
Volume4
Issue number3
StatePublished - May 1 1968

Keywords

  • Blood-borne stimuli
  • Blood-brain barrier
  • Central chemoreceptors
  • Control of respiration
  • Metabolic acidosis
  • Respiratory acidosis
  • Transient hypercapnia
  • Transient infusion

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine

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