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


     

J Appl Physiol 71: 1795-1800, 1991;
8750-7587/91 $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 Hollstien, S. B.
Right arrow Articles by Green, J. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hollstien, S. B.
Right arrow Articles by Green, J. F.

Journal of Applied Physiology, Vol 71, Issue 5 1795-1800, Copyright © 1991 by American Physiological Society

ARTICLES

Role of vagal afferents in the control of abdominal expiratory muscle activity in the dog

S. B. Hollstien, M. L. Carl, E. S. Schelegle and J. F. Green
Department of Human Physiology, School of Medicine, University of California, Davis 95616.

We examined the contribution of afferent vagal A- and C-fibers on abdominal expiratory muscle activity (EMA). In seven spontaneously breathing supine dogs anesthetized with alpha-chloralose we recorded the electromyogram of the external oblique muscle at various vagal temperatures before and after the induction of a pneumothorax. When myelinated fibers were blocked selectively by cooling the vagus nerves to 7 degrees C, EMA decreased to 40% of control (EMA at 39 degrees C). With further cooling to 0 degrees C, removing afferent vagal C-fiber activity, EMA returned to 72% of control. On rewarming the vagus nerves to 39 degrees C, we then induced a pneumothorax (27 ml/kg) that eliminated the EMA in all the dogs studied. Cooling the vagus nerves to 7 degrees C, during the pneumothorax, produced a slight though not significant increase in EMA. However, further cooling of the vagus nerves to 0 degrees C caused the EMA to return vigorously to 116% of control. In three dogs, intravenous infusion of a constant incrementally increasing dose of capsaicin, a C-fiber stimulant, decreased EMA in proportion to the dose delivered. These results suggest that EMA is modulated by a balance between excitatory vagal A-fiber activity, most likely from slowly adapting pulmonary stretch receptors, and inhibitory C-fiber activity, most likely from lung C-fibers.


This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
K.-Z. Lee, D. D. Fuller, I-J. Lu, L.-C. Ku, and J.-C. Hwang
Pulmonary C-fiber receptor activation abolishes uncoupled facial nerve activity from phrenic bursting during positive end-expired pressure in the rat
J Appl Physiol, January 1, 2008; 104(1): 119 - 129.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
J. R. Romaniuk, T. E. Dick, K. E. Kowalski, and A. F. DiMarco
Effects of pulse lung inflation on chest wall expiratory motor activity
J Appl Physiol, January 1, 2007; 102(1): 485 - 491.
[Abstract] [Full Text] [PDF]

Home page
 Br J AnaesthHome page
G. B. Drummond
The abdominal muscles in anaesthesia and after surgery
Br. J. Anaesth., July 1, 2003; 91(1): 73 - 80.
[Full Text] [PDF]


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