PMID- 1890632
OWN - NLM
STAT- MEDLINE
DCOM- 19911015
LR  - 20190510
IS  - 0022-3751 (Print)
IS  - 1469-7793 (Electronic)
IS  - 0022-3751 (Linking)
VI  - 437
DP  - 1991 Jun
TI  - The effects of opiates on the respiratory activity of thoracic motoneurones in 
      the anaesthetized and decerebrate rabbit.
PG  - 181-99
AB  - 1. Efferent discharges were recorded from inspiratory and expiratory intercostal 
      nerve filaments (T2-T10) in artificially ventilated, anaesthetized or decerebrate 
      rabbits with or without vagotomy. 2. Hypocapnic apnoea was used to study the 
      fractional end-tidal CO2 (FET,CO2)-dependent tonic discharges of the expiratory 
      motoneurones, the FET,CO2 threshold for rhythm generation and the FET,CO2 
      response curve of both inspiratory and expiratory burst activity. 3. Incremental 
      doses of morphine (e.g. 1 mg kg-1 I.V.) produced slowing of the respiratory 
      rhythm due to prolongation of the expiratory duration and an elevation of the 
      FET,CO2 threshold for rhythm generation. Eventually apnoea supervened with 
      associated tonic firing of the expiratory motoneurones. At the elevated levels of 
      FET,CO2 bursts of inspiratory activity, with concomitant phasic inhibition of the 
      tonic expiratory activity, could occur either spontaneously or following sensory 
      stimulation. The peak integrated activities of these bursts were closely similar 
      to the values obtained for corresponding levels of FET,CO2 before the 
      administration of morphine. 4. Tonic expiratory activity responded to increased 
      levels of FET,CO2, as it had during hypocapnic apnoea prior to morphine, by an 
      increased discharge frequency of single units or recruitment of new units. 5. All 
      of these effects of morphine were immediately reversed by naloxone (100 
      micrograms kg-1). 6. Naloxone (greater than 100 micrograms kg-1), without 
      pre-treatment with morphine, led to an increase in respiratory frequency due to a 
      shortening of the expiratory duration and a dose-dependent reduction in the 
      FET,CO2 threshold for rhythm generation. There was little alteration either in 
      the inspiratory response to FET,CO2 during rhythm or in the FET,CO2 response of 
      the expiratory output whether expressed as tonic activity during hypocapnic 
      apnoea or phasic activity following the onset of rhythm. 7. Thus opiates act upon 
      the mechanisms of rhythm generation without depressing the FET,CO2 drive as 
      expressed either as phasic or tonic activation of the motoneurones.
FAU - Howard, R S
AU  - Howard RS
AD  - Sobell Department of Neurophysiology, Institute of Neurology, London.
FAU - Sears, T A
AU  - Sears TA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 36B82AMQ7N (Naloxone)
RN  - 76I7G6D29C (Morphine)
SB  - IM
MH  - Animals
MH  - Dose-Response Relationship, Drug
MH  - Inhalation/drug effects
MH  - Male
MH  - Morphine/antagonists & inhibitors/*pharmacology
MH  - Motor Neurons/*drug effects/physiology
MH  - Naloxone/pharmacology
MH  - Rabbits
MH  - Recruitment, Neurophysiological/drug effects
MH  - Respiration/*drug effects
MH  - Thorax/*innervation
MH  - Time Factors
PMC - PMC1180042
EDAT- 1991/06/01 00:00
MHDA- 1991/06/01 00:01
PMCR- 1991/06/01
CRDT- 1991/06/01 00:00
PHST- 1991/06/01 00:00 [pubmed]
PHST- 1991/06/01 00:01 [medline]
PHST- 1991/06/01 00:00 [entrez]
PHST- 1991/06/01 00:00 [pmc-release]
AID - 10.1113/jphysiol.1991.sp018590 [doi]
PST - ppublish
SO  - J Physiol. 1991 Jun;437:181-99. doi: 10.1113/jphysiol.1991.sp018590.