Journal of Applied Physiology  AJP: Regulatory, Integrative and Comparative Physiology
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J Appl Physiol 98: 1125-1139, 2005. First published November 12, 2004; doi:10.1152/japplphysiol.00903.2004
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HIGHLIGHTED TOPICS
Pulmonary Circulation and Hypoxia

Two temporal components within the human pulmonary vascular response to ~2 h of isocapnic hypoxia

Nick P. Talbot,1 George M. Balanos,2 Keith L. Dorrington,1 and Peter A. Robbins1

1University Laboratory of Physiology, University of Oxford, Oxford, and 2School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom

Submitted 19 August 2004 ; accepted in final form 10 November 2004

The time course of the pulmonary vascular response to hypoxia in humans has not been fully defined. In this investigation, study A was designed to assess the form of the increase in pulmonary vascular tone at the onset of hypoxia and to determine whether a steady plateau ensues over the following ~20 min. Twelve volunteers were exposed twice to 5 min of isocapnic euoxia (end-tidal PO2 = 100 Torr), 25 min of isocapnic hypoxia (end-tidal PO2 = 50 Torr), and finally 5 min of isocapnic euoxia. Study B was designed to look for the onset of a slower pulmonary vascular response, and, if possible, to determine a latency for this process. Seven volunteers were exposed to 5 min of isocapnic euoxia, 105 min of isocapnic hypoxia, and finally 10 min of isocapnic euoxia. For both studies, control protocols consisting of isocapnic euoxia were undertaken. Doppler echocardiography was used to measure cardiac output and the maximum tricuspid pressure gradient during systole, and estimates of pulmonary vascular resistance were calculated. For study A, the initial response was well described by a monoexponential process with a time constant of 2.4 ± 0.7 min (mean ± SE). After this, there was a plateau phase lasting at least 20 min. In study B, a second slower phase was identified, with vascular tone beginning to rise again after a latency of 43 ± 5 min. These findings demonstrate the presence of two distinct phases of hypoxic pulmonary vasoconstriction, which may result from two distinct underlying processes.

hypoxic pulmonary vasoconstriction; pulmonary circulation; pulmonary vascular resistance; pulmonary blood flow; cardiac output



Address for reprint requests and other correspondence: P. A. Robbins, University Laboratory of Physiology, Parks Road, Oxford, OX1 3PT, United Kingdom (E-mail: peter.robbins{at}physiol.ox.ac.uk)




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