TY - JOUR
T1 - Neurotransmitters and biphasic respiratory response to hypoxia
AU - Long, W. A.
AU - Lawson, E. E.
PY - 1984
Y1 - 1984
N2 - Recent work from this laboratory (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 55:483-488, 1983) has shown that the biphasic respiratory response to hypoxia in piglets is due to changing central neural respiratory output. To test the hypothesis that either adenosine or opiatelike neurotransmitters mediate the failure to sustain hyperpnea in response to hypoxia, 12 piglets were studied at a mean age of 2.9 ± 0.4 days (range 2-6 days). Animals were anesthetized, paralyzed, and ventilated using a servo-controlled system that maintained end-tidal CO2 constant. Electrical activity of the phrenic nerve was recorded as the index of breathing. An initial experimental trial of 6 min ventilation with 15% O2 was performed in all 12 piglets. Thereafter all 12 piglets were treated with aminophylline (n = 6), naloxone (n = 3), or naltrexone (n = 3) and again subjected to 15% O2. During initial exposure to hypoxia there was an initial increase in phrenic activity that was not sustained. During recovery ventilation with 100% O2, phrenic activity transiently declined below the base-line level and then gradually returned. Subsequent intravenous administration of aminophylline, naloxone, or naltrexone caused base-line phrenic activity to increase. Thereafter repeat exposures to 15% O2 were carried out. During these posttreatment trials of hypoxia, phrenic activity further increased, but the hyperventilation was again not sustained. These findings suggest it is unlikely that either adenosine or μ-endorphin neurotransmitters are the primary mediators of the biphasic response to hypoxia in newborns.
AB - Recent work from this laboratory (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 55:483-488, 1983) has shown that the biphasic respiratory response to hypoxia in piglets is due to changing central neural respiratory output. To test the hypothesis that either adenosine or opiatelike neurotransmitters mediate the failure to sustain hyperpnea in response to hypoxia, 12 piglets were studied at a mean age of 2.9 ± 0.4 days (range 2-6 days). Animals were anesthetized, paralyzed, and ventilated using a servo-controlled system that maintained end-tidal CO2 constant. Electrical activity of the phrenic nerve was recorded as the index of breathing. An initial experimental trial of 6 min ventilation with 15% O2 was performed in all 12 piglets. Thereafter all 12 piglets were treated with aminophylline (n = 6), naloxone (n = 3), or naltrexone (n = 3) and again subjected to 15% O2. During initial exposure to hypoxia there was an initial increase in phrenic activity that was not sustained. During recovery ventilation with 100% O2, phrenic activity transiently declined below the base-line level and then gradually returned. Subsequent intravenous administration of aminophylline, naloxone, or naltrexone caused base-line phrenic activity to increase. Thereafter repeat exposures to 15% O2 were carried out. During these posttreatment trials of hypoxia, phrenic activity further increased, but the hyperventilation was again not sustained. These findings suggest it is unlikely that either adenosine or μ-endorphin neurotransmitters are the primary mediators of the biphasic response to hypoxia in newborns.
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U2 - 10.1152/jappl.1984.57.1.213
DO - 10.1152/jappl.1984.57.1.213
M3 - Article
C2 - 6147336
AN - SCOPUS:0021142595
SN - 0161-7567
VL - 57
SP - 213
EP - 222
JO - Journal of Applied Physiology Respiratory Environmental and Exercise Physiology
JF - Journal of Applied Physiology Respiratory Environmental and Exercise Physiology
IS - 1
ER -