Journal of Applied Physiology Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 77: 236-244, 1994;
8750-7587/94 $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 Yanos, J.
Right arrow Articles by Banner, A. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yanos, J.
Right arrow Articles by Banner, A. S.

Journal of Applied Physiology, Vol 77, Issue 1 236-244, Copyright © 1994 by American Physiological Society

ARTICLES

Mechanism of respiratory arrest in an animal model of acute fatal bronchoconstriction

J. Yanos, M. J. Patti and A. S. Banner
Department of Medicine, University of Missouri, Columbia 65212.

The cause of respiratory arrest in acute asthma is not known. By its nature, respiratory arrest is difficult to study clinically. The possible causes of respiratory arrest include cardiovascular dysfunction, respiratory muscle fatigue, and central respiratory failure. We used a dog model of respiratory arrest in acute bronchoconstriction that examined the effects of hypoxemia and intrinsic loading in an attempt to establish the mechanism. Our hypothesis was that, in a setting of hypoxemia and intrinsic loading similar to human fatal asthma, respiratory arrest is caused by a central respiratory failure, more specifically, failure of the central rhythm generator. We studied 18 dogs divided into 1) an intrinsically loaded group, 2) a hypoxemic group, and 3) both a loaded and a hypoxemic group. Intrinsic loading was induced with methacholine combined with selective beta 2-blockade, and the hypoxemia was controlled by varying inspired O2 fraction. Respiratory arrest occurred only in animals with both hypoxemia and intrinsic loading. We found no evidence of hemodynamic instability or respiratory muscle fatigue. Instead, there was an abrupt cessation of ventilation while the intensity of the central neural output was maintained. Our results are consistent with a failure of the central rhythm generator as the causal agent in respiratory arrest.


This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
J. A. Simpson and S. Iscoe
Cardiorespiratory failure in rat induced by severe inspiratory resistive loading
J Appl Physiol, April 1, 2007; 102(4): 1556 - 1564.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
J. A. Simpson, J. Van Eyk, and S. Iscoe
Respiratory muscle injury, fatigue and serum skeletal troponin I in rat
J. Physiol., February 1, 2004; 554(3): 891 - 903.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
D. K. McKenzie, G. M. Allen, J. E. Butler, and S. C. Gandevia
Task failure with lack of diaphragm fatigue during inspiratory resistive loading in human subjects
J Appl Physiol, June 1, 1997; 82(6): 2011 - 2019.
[Abstract] [Full Text] [PDF]


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