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


     

J Appl Physiol 45: 33-39, 1978;
8750-7587/78 $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 Hales, C. A.
Right arrow Articles by Slate, J. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hales, C. A.
Right arrow Articles by Slate, J. L.

Journal of Applied Physiology, Vol 45, Issue 1 33-39, Copyright © 1978 by American Physiological Society

ARTICLES

Influence of aspirin and indomethacin on variability of alveolar hypoxic vasoconstriction

C. A. Hales, E. T. Rouse and J. L. Slate

Alveolar hypoxia induces pulmonary vasoconstriction but the strength of alveolar hypoxic vasoconstriction (AHV) is variable even within the same species. The influence of aspirin and indomethacin, cyclo-oxygenase inhibitors, was examined in two groups of dogs, those with weak AHV and those with vigorous AHV. A double-lumen endotracheal tube allowed ventilation of one lung with nitrogen as an alveolar hypoxic stimulus and ventilation of the other lung with O2 to maintain systemic oxygenation. Perfusion to each lung was measured with xenon-133 and external counters. In weak reactors both aspirin and indomethacin induced fourfold enhancement of AHV (P less than 0.01), whereas no significant influence on vigorous reactors was noted. Cyclo-oxygenase inhibitors also produced enhanced reactivity in the isolated lung to alveolar hypoxia and prostaglandin F2alpha but not to angiotensin II and norepinephrine. Aspirin-enhanced AHV in the isolated lung could not be diminished with blockade of angiotensin II receptors or of alpha receptors. In summary, weak AHV in intact or isolated dog lung may be due to an excess of a prostaglandin or prostacyclin vasodilator.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
H. C. Champion, D. J. Villnave, A. Tower, P. J. Kadowitz, and A. L. Hyman
A novel right-heart catheterization technique for in vivo measurement of vascular responses in lungs of intact mice
Am J Physiol Heart Circ Physiol, January 1, 2000; 278(1): H8 - H15.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
S. Mink, A. Becker, S. Sharma, H. Unruh, K. Duke, and W. Kepron
Role of autacoids in cardiovascular collapse in anaphylactic shock in anesthetized dogs
Cardiovasc Res, July 1, 1999; 43(1): 173 - 182.
[Abstract] [Full Text] [PDF]

Home page
 SEMIN CARDIOTHORAC VASC ANESTHHome page
M. L. Fisher and S. C. Body
Physiology of One-Lung Ventilation
Seminars in Cardiothoracic and Vascular Anesthesia, September 1, 1997; 1(3): 236 - 255.
[Abstract] [PDF]


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