Naloxone enhances respiratory output in cats

E. E. Lawson, T. G. Waldrop, F. L. Eldridge

Research output: Contribution to journalArticlepeer-review

Abstract

To investigate the physiological role of opiate receptors and opiatelike neurotransmitters, which are present in brain-stem respiratory centers, we administered naloxone to 10 cats by intravenous injection. These animals were vagotomized, paralyzed, and servo-ventilated to maintain constant end-tidal CO2; in addition, their carotid sinus nerves were sectioned bilaterally. Respiratory output was assessed by integration of phrenic nerve activity. Control saline infusions had no effect on respiratory output. However, administration of naloxone (0.4 mg/kg) caused phrenic minute output to increase significantly in each of five anesthetized cerebrate cats (control 7,272 ± 1.615 U/min; 30 min postnaloxone 12,920 ± 3,857 U/min; P < 0.05) and five unanesthetized decerebrate cats (control 10,368 ± 1,222 U/min; naloxone 14,648 ± 3,225 U/min; P < 0.05). In addition to the effect on phrenic minute output, naloxone infusion resulted in an increase of the inspiratory rate of rise of phrenic nerve activity in each cat. There was no change in the ratio of inspiratory duration to total respiratory period (TI/Ttot). Because naloxone is a specific opiate antagonist, we suggest that endogenous opiatelike neurotransmitters (endorphins) may modulate central inspiratory drive.

Original languageEnglish (US)
Pages (from-to)1105-1111
Number of pages7
JournalJournal of Applied Physiology Respiratory Environmental and Exercise Physiology
Volume47
Issue number5
DOIs
StatePublished - Jan 1 1979
Externally publishedYes

ASJC Scopus subject areas

  • Physiology
  • Endocrinology

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