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


     

J Appl Physiol 51: 755-761, 1981;
8750-7587/81 $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 Herget, J.
Right arrow Articles by Petrovicka, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Herget, J.
Right arrow Articles by Petrovicka, M.

Journal of Applied Physiology, Vol 51, Issue 3 755-761, Copyright © 1981 by American Physiological Society

ARTICLES

Pulmonary hypertension induced by repeated pulmonary inflammation in the rat

J. Herget, F. Palecek, P. Preclik, M. Cermakova, M. Vizek and M. Petrovicka

The effect of repeated lung inflammation on the pulmonary vascular bed was studied in rats. Nonbacterial lung inflammation was induced by repeated carrageenan instillations into the lungs. Three days after the single carrageenan injection, the mean pulmonary arterial blood pressure was only slightly raised [16.3 +/- 0.6 (mean +/- SE) Torr in controls and 19.5 +/- 0.5 Torr in rats with lung inflammation, P less than 0.001]. A substantial pulmonary hypertension was found in rats 3 days after the sixth lung inflammation (24.6 +/- 1 Torr). In this group, arterial hypoxemia, hypercapnia, and right-heart hypertrophy were found. In the 14th day of recovery after the last injection of carrageenan, the mean pulmonary artery blood pressure decreased (18.5 +/- 0.9 Torr) but remained higher than in the control group. There was no difference in cardiac output measured by dye-dilution technique between the experimental and control groups. After repeated inflammation, the media of distal pulmonary vessels thickened and the number of pulmonary arterioles with distinct media increased.


This article has been cited by other articles:


Home page
 J Trop PediatrHome page
A. Uner, M. Dogan, M. Demirtas, M. Acikgoz, H. Temel, A. Kaya, and H. Caksen
Comparison of Nifedipine and Captopril in Children with Pulmonary Hypertension due to Broncopneumonia
J Trop Pediatr, February 26, 2008; (2008) fmn012v1.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
V. Hampl and J. Herget
Role of Nitric Oxide in the Pathogenesis of Chronic Pulmonary Hypertension
Physiol Rev, October 1, 2000; 80(4): 1337 - 1372.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
L. WRIGHT, R. M. TUDER, J. WANG, C. D. COOL, R. A. LEPLEY, and N. F. VOELKEL
5-Lipoxygenase and 5-Lipoxygenase Activating Protein (FLAP) Immunoreactivity in Lungs from Patients with Primary Pulmonary Hypertension
Am. J. Respir. Crit. Care Med., January 1, 1997; 157(1): 219 - 229.
[Abstract] [Full Text]


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