Ventilatory responses to specific CNS hypoxia in sleeping dogs
The John Rankin Laboratory of Pulmonary Medicine, Department of Preventive Medicine, University of Wisconsin, Madison, Wisconsin 53705 Our study was concerned with the effect of brain hypoxia on cardiorespiratory control in the sleeping dog. Eleven unanesthetized dogs were studied; seven were prepar...
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Published in: | Journal of applied physiology (1985) Vol. 88; no. 5; pp. 1840 - 1852 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Bethesda, MD
Am Physiological Soc
01-05-2000
American Physiological Society |
Subjects: | |
Online Access: | Get full text |
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Summary: | The John Rankin Laboratory of Pulmonary Medicine, Department of
Preventive Medicine, University of Wisconsin, Madison, Wisconsin 53705
Our study was concerned with the effect of brain hypoxia
on cardiorespiratory control in the sleeping dog. Eleven unanesthetized dogs were studied; seven were prepared for vascular isolation and
extracorporeal perfusion of the carotid body to assess the effects of
systemic [and, therefore, central nervous system (CNS)] hypoxia (arterial P O 2 = 52, 45, and
38 Torr) in the presence of a normocapnic, normoxic, and normohydric
carotid body during non-rapid eye movement sleep. A lack of ventilatory
response to systemic boluses of sodium cyanide during carotid body
perfusion demonstrated isolation of the perfused carotid body and lack
of other significant peripheral chemosensitivity. Four additional dogs
were carotid body denervated and exposed to whole body hypoxia for
comparison. In the sleeping dog with an intact and perfused carotid
body exposed to specific CNS hypoxia, we found the following. 1 ) CNS hypoxia for 5-25 min resulted in modest but
significant hyperventilation and hypocapnia (minute ventilation
increased 29 ± 7% at arterial
P O 2 = 38 Torr); carotid
body-denervated dogs showed no ventilatory response to hypoxia.
2 ) The hyperventilation was caused by increased breathing
frequency. 3 ) The hyperventilatory response developed rapidly
(<30 s). 4 ) Most dogs maintained hyperventilation for up to
25 min of hypoxic exposure. 5 ) There were no significant changes in blood pressure or heart rate. We conclude that specific CNS
hypoxia, in the presence of an intact carotid body maintained normoxic
and normocapnic, does not depress and usually stimulates breathing
during non-rapid eye movement sleep. The rapidity of the response
suggests a chemoreflex meditated by hypoxia-sensitive respiratory-related neurons in the CNS.
carotid body; hypoxic depression; chemoreceptors; hypocapnia |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 8750-7587 1522-1601 |
DOI: | 10.1152/jappl.2000.88.5.1840 |