Journal of Applied Physiology http://www.adinstruments.com/labchart/faseb
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 65: 736-743, 1988;
8750-7587/88 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Melton, J. E.
Right arrow Articles by Edelman, N. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Melton, J. E.
Right arrow Articles by Edelman, N. H.

Journal of Applied Physiology, Vol 65, Issue 2 736-743, Copyright © 1988 by American Physiological Society

ARTICLES

CO2 sensitivity of cat phrenic neurogram during hypoxic respiratory depression

J. E. Melton, J. A. Neubauer and N. H. Edelman
Department of Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick 08903-0019.

The CO2 response of the phrenic neurogram before and during CO-induced isocapnic brain hypoxia was studied in peripherally chemodenervated, vagotomized, paralyzed, ventilated cats with blood pressure held constant. During inhalation of 0.5% CO in 40% O2, arterial O2 content (CaO2) was reduced to 40% and minute phrenic activity to 38.4 +/- 9.4% (SE; n = 9) of prehypoxic levels, primarily due to depression of peak phrenic amplitude (PP). CO2 response, defined as the slope of the plot of PP vs. end-tidal PCO2 during CO2 rebreathing, was unaffected by phrenic depression even to the point of total suppression of phrenic activity in two cats. The effect of the tissue metabolic acidosis associated with hypoxia on phrenic CO2 sensitivity was assessed in a separate group of cats by blocking lactate formation during hypoxia with dichloroacetate (DCA). Preventing lactic acidosis during hypoxia did not affect the CO2 response of the phrenic activity during hypoxia. We conclude that 1) hypoxic depression does not limit the ability of central respiratory neurons to respond to CO2, and 2) the failure of DCA to affect the CO2 response of the phrenic neurogram suggests that brain intracellular lactic acidosis does not modify the phrenic response to hypercapnia.


This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
A. K. Curran, J. R. Rodman, P. R. Eastwood, K. S. Henderson, J. A. Dempsey, and C. A. Smith
Ventilatory responses to specific CNS hypoxia in sleeping dogs
J Appl Physiol, May 1, 2000; 88(5): 1840 - 1852.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
H. Gautier, C. Murariu, and M. Bonora
Ventilatory and metabolic responses to ambient hypoxia or hypercapnia in rats exposed to CO hypoxia
J Appl Physiol, July 1, 1997; 83(1): 253 - 261.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online