TY - JOUR
T1 - Naloxone enhances respiratory output in cats
AU - Lawson, E. E.
AU - Waldrop, T. G.
AU - Eldridge, F. L.
PY - 1979
Y1 - 1979
N2 - 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.
AB - 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.
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U2 - 10.1152/jappl.1979.47.5.1105
DO - 10.1152/jappl.1979.47.5.1105
M3 - Article
C2 - 511712
AN - SCOPUS:0018688040
SN - 0161-7567
VL - 47
SP - 1105
EP - 1111
JO - Journal of Applied Physiology Respiratory Environmental and Exercise Physiology
JF - Journal of Applied Physiology Respiratory Environmental and Exercise Physiology
IS - 5
ER -