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


     

J Appl Physiol 72: 447-454, 1992;
8750-7587/92 $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 Teitelbaum, J. S.
Right arrow Articles by Hussain, S. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Teitelbaum, J. S.
Right arrow Articles by Hussain, S. N.

Journal of Applied Physiology, Vol 72, Issue 2 447-454, Copyright © 1992 by American Physiological Society

ARTICLES

Effects of diaphragmatic ischemia on the inspiratory motor drive

J. S. Teitelbaum, S. A. Magder, C. Roussos and S. N. Hussain
Critical Care Division, Royal Victoria Hospital, Montreal, Quebec, Canada.

To assess the effect of diaphragmatic ischemia on the inspiratory motor drive, we studied the in situ isolated and innervated left diaphragm in anesthetized, vagotomized, and mechanically ventilated dogs. The arterial and venous vessels of the left diaphragm were catheterized and isolated from the systemic circulation. Inspiratory muscle activation was assessed by recording the integrated electromyographic (EMG) activity of the left and right costal diaphragms and parasternal intercostal and alae nasi muscles. Tension generated by the left diaphragm during spontaneous breathing attempts was also measured. In eight animals, left diaphragmatic ischemia was induced by occluding the phrenic artery for 20 min, followed by 10 min of reperfusion. This elicited a progressive increase in EMG activity of the left and right diaphragms and parasternal and alae nasi muscles to 170, 157, 152, and 128% of baseline values, respectively, an increase in the frequency of breathing efforts, and no change in left diaphragmatic spontaneous tension. Thus the ratio of left diaphragmatic EMG to tension rose progressively during ischemia. During reperfusion, only the frequency of breathing efforts and alae nasi EMG recovered completely. In four additional animals, left diaphragmatic ischemia was induced after the left phrenic nerve was sectioned. Neither EMG activity of inspiratory muscles nor respiratory timing changed significantly during ischemia. In conclusion, diaphragmatic ischemia increases inspiratory motor drive through activation of phrenic afferents. The changes in alae nasi activity and respiratory timing indicate that this influence is achieved through supraspinal pathways.


This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
J. R. Rodman, K. S. Henderson, C. A. Smith, and J. A. Dempsey
Cardiovascular effects of the respiratory muscle metaboreflexes in dogs: rest and exercise
J Appl Physiol, September 1, 2003; 95(3): 1159 - 1169.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
H. V. Forster
Plasticity in Respiratory Motor Control: Invited Review: Plasticity in the control of breathing following sensory denervation
J Appl Physiol, February 1, 2003; 94(2): 784 - 794.
[Abstract] [Full Text] [PDF]


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