Journal of Applied Physiology Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 55: 1486-1495, 1983;
8750-7587/83 $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 Musch, T. I.
Right arrow Articles by Bateman, N. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Musch, T. I.
Right arrow Articles by Bateman, N. T.

Journal of Applied Physiology, Vol 55, Issue 5 1486-1495, Copyright © 1983 by American Physiological Society

ARTICLES

Metabolic acids and [H+] regulation in brain tissue during acclimatization to chronic hypoxia

T. I. Musch, J. A. Dempsey, C. A. Smith, G. S. Mitchell and N. T. Bateman

Ventilatory acclimatization, arterial acid-base status, brain stem and cortex metabolic acids, and high-energy phosphates were determined in rats during 2-h to 7-days exposure to two levels of hypoxia (O2 inspiratory pressure 75 and 58 Torr), and upon acute restoration of normoxia. Brain lactate concentrations increased during acute exposure to both moderate hypoxia (+52% in cortex and +61% in stem) and severe hypoxia (+211% in cortex and +163% in stem), and during chronic hypoxia remained unchanged or decreased, respectively, as hyperventilation progressed and arterial O2 content rose. Restoration of normoxia after chronic hypoxic exposure resulted in continued hyperventilation and elevated lactate concentrations. Brain intracellular pH was unchanged throughout moderate hypoxia and during severe hypoxia, became acid during acute exposure, but was completely compensated after 72 h of continued hypoxia. Preventing the hypocapnia (via increased inspiratory fraction of CO2) during acute hypoxia or restoring normocapnia during posthypoxic normoxia revealed the effects of hypocapnia independently of hypoxemia. Hypocapnia accounted for all of the changes in brain lactate concentration during moderate hypoxia but only 40-60% of the lactate changes during severe hypoxia. We speculate that the observed changes in plasma and brain tissue metabolic acids and in plasma [HCO-3] would acidify cerebral interstitial fluid (ISF) in chronic hypoxia; however, the time course of this change in ISF acid-base status would be quite different between the two levels of hypoxia and uncorrelated with the patterns of ventilatory acclimatization.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
L.-M. Chen, I. Choi, G. G. Haddad, and W. F. Boron
Chronic continuous hypoxia decreases the expression of SLC4A7 (NBCn1) and SLC4A10 (NCBE) in mouse brain
Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2007; 293(6): R2412 - R2420.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
K. Xu and J. C. LaManna
Chronic hypoxia and the cerebral circulation
J Appl Physiol, February 1, 2006; 100(2): 725 - 730.
[Abstract] [Full Text] [PDF]


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