help button home button
AJRCCM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Vejlstrup, N. G.
Right arrow Articles by Dorrington, K. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Vejlstrup, N. G.
Right arrow Articles by Dorrington, K. L.

Am. J. Respir. Crit. Care Med., Vol 155, No. 1, 01 1997, 216-221.

Time course of hypoxic pulmonary vasoconstriction: a rabbit model of regional hypoxia

NG Vejlstrup, M O'Neill, B Nagyova and KL Dorrington
University Laboratory of Physiology, Oxford, England, United Kingdom.

There is disagreement in the literature about the time required for hypoxic constriction of pulmonary vessels to reach its full intensity. Some studies suggest that only minutes are required, others that several hours are needed. We examined the time course over 6 h of changes in pulmonary shunt (as a fraction of cardiac output) following induction of unilateral hypoxia by collapse or liquid filling of the left lung in 47 anesthetized rabbits. The time course was examined at four degrees of lung inflation: during collapse and at airway pressures of 0.3 kPa, 0.6 kPa, and 0.9 kPa. The respective volumes (mean +/- SD) of the liquid-filled lung were estimated to be 6.4 +/- 1.0, 12.8 +/- 2.5, and 15.8 +/- 1.6 ml/kg body weight (BW). During sustained hypoxia (the period from 150 to 360 min after inducing hypoxia), shunt declined at a slow linear rate of 2.37 x 10(-4)/min, which was independent of lung inflation (p = 0.65 analysis of variance [ANOVA]) and significantly different from zero (p < 0.001). The stability of cardiac output in this animal model, as measured sequentially by thermodilution, was confirmed in a further 20 animals. The experiments provide evidence for a slow intensification of blood-flow diversion at a rate that does not depend upon the degree of lung inflation. Whether this change is a feature of hypoxic constriction itself, or some modulation of it, remains unclear.


This article has been cited by other articles:


Home page
Am. J. Respir. Cell Mol. Bio.Home page
N. Weissmann, S. Zeller, R. U. Schafer, C. Turowski, M. Ay, K. Quanz, H. A. Ghofrani, R. T. Schermuly, L. Fink, W. Seeger, et al.
Impact of Mitochondria and NADPH Oxidases on Acute and Sustained Hypoxic Pulmonary Vasoconstriction
Am. J. Respir. Cell Mol. Biol., April 1, 2006; 34(4): 505 - 513.
[Abstract] [Full Text] [PDF]


Home page
Br J AnaesthHome page
B. Nagyova, M. O'Neill, and K. L. Dorrington
Inhibition of active sodium absorption leads to a net liquid secretion into in vivo rabbit lung at two levels of alveolar hypoxia
Br. J. Anaesth., December 1, 2001; 87(6): 897 - 904.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
N. Weissmann, S. Winterhalder, M. Nollen, R. Voswinckel, K. Quanz, H. A. Ghofrani, R. T. Schermuly, W. Seeger, and F. Grimminger
NO and reactive oxygen species are involved in biphasic hypoxic vasoconstriction of isolated rabbit lungs
Am J Physiol Lung Cell Mol Physiol, April 1, 2001; 280(4): L638 - L645.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 1997 American Thoracic Society
  ATS 2008 State of the Art Course