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


     


J Appl Physiol 49: 52-58, 1980;
8750-7587/80 $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 Google Scholar
Google Scholar
Right arrow Articles by Leitch, A. G.
Right arrow Articles by Loudon, R. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Leitch, A. G.
Right arrow Articles by Loudon, R. G.

Journal of Applied Physiology, Vol 49, Issue 1 52-58, Copyright © 1980 by American Physiological Society


ARTICLES

Ventilatory response to transient hyperoxia in head injury hyperventilation

A. G. Leitch, J. E. McLennan, S. Balkenhol, R. L. McLaurin and R. G. Loudon

We have measured breath-by-breath instantaneous minute ventilation (VIinst) before, during, and after the administration of 10 breaths of 100% oxygen to seven male patients with head injury hyperventilation. The patients were hypoxemic (PaO2 61.2 +/- 6.3) and hypocapnic (PaCO2 26.6 +/- 5.9) with a respiratory alkalosis (pH 7.53 +/- 0.06) while breathing air. Following the oxygen VIinst fell on the average by 40 +/- 12.7% from 16.06 +/- 3.75 1.min-1 to a minimum of 9.73 +/- 3.20 1.min-1 at 20.4 +/- 2.9 s after the first breath of oxygen. In the majority of our hyperventilating patients, almost all of the resting hyperventilation could be abolished transiently by 100% oxygen. This fall in ventilation represents the peripheral chemoreceptor contribution to resting ventilation and is increased in the head injury patients in comparison with normal subjects breathing air or hypoxic gas mixtures, altitude-acclimatized subjects and patients who are hypoxic because of chronic bronchitis or interstitial lung disease. We suggest that the increased reflex hypoxic drive to ventilation found in our patients is secondary to their cerebral injury, resulting in a reduction of descending cortical inhibitory influences on the medullary respiratory control centers.





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