Carotid sinus nerve responses and ventilatory acclimatization to hypoxia in adult rats following 2 weeks of postnatal hyperoxia
Adult rats have decreased carotid body volume and reduced carotid sinus nerve, phrenic nerve, and ventilatory responses to acute hypoxic stimulation after exposure to postnatal hyperoxia (60% O 2, PNH) during the first 4 weeks of life. Moreover, sustained hypoxic exposure (12%, 7 days) partially rev...
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Published in: | Respiratory physiology & neurobiology Vol. 150; no. 2; pp. 155 - 164 |
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Abstract | Adult rats have decreased carotid body volume and reduced carotid sinus nerve, phrenic nerve, and ventilatory responses to acute hypoxic stimulation after exposure to postnatal hyperoxia (60% O
2, PNH) during the first 4 weeks of life. Moreover, sustained hypoxic exposure (12%, 7 days) partially reverses functional impairment of the acute hypoxic phrenic nerve response in these rats. Similarly, 2 weeks of PNH results in the same phenomena as above except that ventilatory responses to acute hypoxia have not been measured in awake rats. Thus, we hypothesized that 2-week PNH-treated rats would also exhibit blunted chemoafferent responses to acute hypoxia, but would exhibit ventilatory acclimatization to sustained hypoxia. Rats were born into, and exposed to PNH for 2 weeks, followed by chronic room-air exposure. At 3–4 months of age, two studies were performed to assess: (1) carotid sinus nerve responses to asphyxia and sodium cyanide in anesthetized rats and (2) ventilatory and blood gas responses in awake rats before (d0), during (d1 and d7), and 1 day following (d8) sustained hypoxia. Carotid sinus nerve responses to i.v. NaCN and asphyxia (10
s) were significantly reduced in PNH-treated versus control rats; however, neither the acute hypoxic ventilatory response nor the time course or magnitude of ventilatory acclimatization differed between PNH and control rats despite similar levels of
P
a
O
2
. Although carotid body volume was reduced in PNH rats, carotid body volumes increased during sustained hypoxia in both PNH and control rats. We conclude that normal acute and chronic ventilatory responses are related to retained (though impaired) carotid body chemoafferent function combined with central neural mechanisms which may include brainstem hypoxia-sensitive neurons and/or brainstem integrative plasticity relating both central and peripheral inputs. |
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AbstractList | Adult rats have decreased carotid body volume and reduced carotid sinus nerve, phrenic nerve, and ventilatory responses to acute hypoxic stimulation after exposure to postnatal hyperoxia (60% O2, PNH) during the first 4 weeks of life. Moreover, sustained hypoxic exposure (12%, 7 days) partially reverses functional impairment of the acute hypoxic phrenic nerve response in these rats. Similarly, 2 weeks of PNH results in the same phenomena as above except that ventilatory responses to acute hypoxia have not been measured in awake rats. Thus, we hypothesized that 2-week PNH-treated rats would also exhibit blunted chemoafferent responses to acute hypoxia, but would exhibit ventilatory acclimatization to sustained hypoxia. Rats were born into, and exposed to PNH for 2 weeks, followed by chronic room-air exposure. At 3-4 months of age, two studies were performed to assess: (1) carotid sinus nerve responses to asphyxia and sodium cyanide in anesthetized rats and (2) ventilatory and blood gas responses in awake rats before (d0), during (d1 and d7), and 1 day following (d8) sustained hypoxia. Carotid sinus nerve responses to i.v. NaCN and asphyxia (10 s) were significantly reduced in PNH-treated versus control rats; however, neither the acute hypoxic ventilatory response nor the time course or magnitude of ventilatory acclimatization differed between PNH and control rats despite similar levels of PaO2 . Although carotid body volume was reduced in PNH rats, carotid body volumes increased during sustained hypoxia in both PNH and control rats. We conclude that normal acute and chronic ventilatory responses are related to retained (though impaired) carotid body chemoafferent function combined with central neural mechanisms which may include brainstem hypoxia-sensitive neurons and/or brainstem integrative plasticity relating both central and peripheral inputs. Adult rats have decreased carotid body volume and reduced carotid sinus nerve, phrenic nerve, and ventilatory responses to acute hypoxic stimulation after exposure to postnatal hyperoxia (60% O 2, PNH) during the first 4 weeks of life. Moreover, sustained hypoxic exposure (12%, 7 days) partially reverses functional impairment of the acute hypoxic phrenic nerve response in these rats. Similarly, 2 weeks of PNH results in the same phenomena as above except that ventilatory responses to acute hypoxia have not been measured in awake rats. Thus, we hypothesized that 2-week PNH-treated rats would also exhibit blunted chemoafferent responses to acute hypoxia, but would exhibit ventilatory acclimatization to sustained hypoxia. Rats were born into, and exposed to PNH for 2 weeks, followed by chronic room-air exposure. At 3–4 months of age, two studies were performed to assess: (1) carotid sinus nerve responses to asphyxia and sodium cyanide in anesthetized rats and (2) ventilatory and blood gas responses in awake rats before (d0), during (d1 and d7), and 1 day following (d8) sustained hypoxia. Carotid sinus nerve responses to i.v. NaCN and asphyxia (10 s) were significantly reduced in PNH-treated versus control rats; however, neither the acute hypoxic ventilatory response nor the time course or magnitude of ventilatory acclimatization differed between PNH and control rats despite similar levels of P a O 2 . Although carotid body volume was reduced in PNH rats, carotid body volumes increased during sustained hypoxia in both PNH and control rats. We conclude that normal acute and chronic ventilatory responses are related to retained (though impaired) carotid body chemoafferent function combined with central neural mechanisms which may include brainstem hypoxia-sensitive neurons and/or brainstem integrative plasticity relating both central and peripheral inputs. |
Author | Mitchell, Gordon S. Bisgard, Gerald E. Wang, Zunyi Keith, Ingegerd M. Wenninger, Julie M. Olson, E. Burt |
Author_xml | – sequence: 1 givenname: Julie M. surname: Wenninger fullname: Wenninger, Julie M. email: wenninger@svm.vetmed.wisc.edu organization: Department of Comparative Biosciences, University of Wisconsin-Madison, School of Veterinary Medicine, 2015 Linden Dr, Madison, WI 53706, USA – sequence: 2 givenname: E. Burt surname: Olson fullname: Olson, E. Burt organization: Department of Population Health Sciences, University of Wisconsin-Madison, Madison, WI 53706, USA – sequence: 3 givenname: Zunyi surname: Wang fullname: Wang, Zunyi organization: Department of Comparative Biosciences, University of Wisconsin-Madison, School of Veterinary Medicine, 2015 Linden Dr, Madison, WI 53706, USA – sequence: 4 givenname: Ingegerd M. surname: Keith fullname: Keith, Ingegerd M. organization: Department of Comparative Biosciences, University of Wisconsin-Madison, School of Veterinary Medicine, 2015 Linden Dr, Madison, WI 53706, USA – sequence: 5 givenname: Gordon S. surname: Mitchell fullname: Mitchell, Gordon S. organization: Department of Comparative Biosciences, University of Wisconsin-Madison, School of Veterinary Medicine, 2015 Linden Dr, Madison, WI 53706, USA – sequence: 6 givenname: Gerald E. surname: Bisgard fullname: Bisgard, Gerald E. organization: Department of Comparative Biosciences, University of Wisconsin-Madison, School of Veterinary Medicine, 2015 Linden Dr, Madison, WI 53706, USA |
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Cites_doi | 10.1152/jappl.1999.87.2.817 10.1113/jphysiol.2001.012908 10.1111/j.1469-7793.1998.519bn.x 10.1046/j.1460-9568.2000.00208.x 10.1152/japplphysiol.01043.2002 10.1152/jappl.1978.44.5.763 10.1152/japplphysiol.00831.2003 10.1152/japplphysiol.00819.2001 10.1152/jappl.1999.87.6.2128 10.1152/ajpregu.2000.279.5.R1625 10.1152/japplphysiol.00985.2002 10.1016/j.resp.2004.10.008 10.1113/jphysiol.1996.sp021616 10.1152/jappl.1988.64.2.666 10.1016/0034-5687(87)90029-6 10.1152/japplphysiol.00859.2001 10.1111/j.1469-7793.2001.00917.x 10.1152/jn.2000.83.5.2854 10.1038/nn0901-927 10.1002/jemt.10191 10.1152/japplphysiol.00953.2003 |
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Keywords | Neuroplasticity Development Hypoxia Respiratory control Carotid body Ventilatory acclimatization Peripheral chemoreceptors Human Oxygen Rat Rodentia Respiratory system Chemoreceptor Vertebrata Mammalia Postnatal Ventilatory response Hyperoxia Adult Carotid sinus |
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SubjectTerms | Acclimatization - physiology Animals Animals, Newborn Asphyxia - physiopathology Biological and medical sciences Blood Gas Analysis - methods Cardiorespiratory control. Arterial mecano- and chemoreceptor Carotid body Carotid Sinus - physiopathology Development Enzyme Inhibitors - pharmacology Female Fundamental and applied biological sciences. Psychology Hyperoxia - physiopathology Hypoxia Hypoxia - physiopathology Male Neuroplasticity Partial Pressure Peripheral chemoreceptors Phrenic Nerve - drug effects Phrenic Nerve - physiopathology Pregnancy Pulmonary Ventilation - physiology Rats Rats, Sprague-Dawley Respiratory control Sodium Cyanide - pharmacology Time Factors Ventilatory acclimatization Vertebrates: respiratory system |
Title | Carotid sinus nerve responses and ventilatory acclimatization to hypoxia in adult rats following 2 weeks of postnatal hyperoxia |
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