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


     

J Appl Physiol 60: 918-927, 1986;
8750-7587/86 $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 Phipps, R. J.
Right arrow Articles by Wanner, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Phipps, R. J.
Right arrow Articles by Wanner, A.

Journal of Applied Physiology, Vol 60, Issue 3 918-927, Copyright © 1986 by American Physiological Society

ARTICLES

Effects of 0.5 ppm ozone on glycoprotein secretion, ion and water fluxes in sheep trachea

R. J. Phipps, S. M. Denas, M. W. Sielczak and A. Wanner

We studied the effects of ozone (O3) exposure on airway mucus secretion. Sheep were exposed in vivo to 0.5 ppm O3, 4 h/day for 2 days (acute, n = 6), 6 wks (chronic, n = 6) or 6 wks + 1 wk recovery (chronic + recovery, n = 6). Secretion of glycoproteins (radiolabeled with 35SO4 and [3H]threonine), and transepithelial fluxes of Cl-, Na+ and water were subsequently measured in tracheal tissues in vitro, and were compared with values from control, unexposed sheep (n = 8). Acute O3 exposure increased basal secretion of sulfated glycoproteins (P less than 0.05), but had no effect on ion fluxes. Chronic exposure reduced basal glycoprotein secretion, but increased net Cl- secretion. Under open-circuit conditions, chronic exposure also induced net water secretion (P less than 0.05). With 7 days recovery, basal glycoprotein secretion (predominantly sulfated) was greatly increased above control, while the increased net secretion of Cl- and of water persisted (P less than 0.05). Histology of the airways indicated that acute exposure induced moderate hypertrophy of submucosal glands in the lower trachea (P less than 0.05), while chronic exposure (with and without recovery) induced a large hypertrophy of submucosal glands in both upper and lower trachea (P less than 0.05). Without recovery, however, the gland cells were devoid of secretory material, whereas with recovery they were full of secretory material. This suggests that the decreased glycoprotein secretion with chronic exposure alone resulted from incomplete replenishment of intracellular stores after 6 wks of stimulation. We conclude that both short- and long-term O3 exposure causes airway-mucus hypersecretion.


This article has been cited by other articles:


Home page
 Eur Respir JHome page
L.G. Wood, P.G. Gibson, and M.L. Garg
Biomarkers of lipid peroxidation, airway inflammation and asthma
Eur. Respir. J., January 1, 2003; 21(1): 177 - 186.
[Abstract] [Full Text] [PDF]


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