Proceedings of The Physiological Society

University College Cork (2004) J Physiol 560P, C21



Talbot,Nick P; Balanos,George M; Dorrington,Keith L; Robbins,Peter A;

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

  • ∆Pmax and cardiac output during hypoxia and control protocols (mean±SEM n=7). Filled circles indicate values during hypoxia.

Pulmonary vasoconstriction during hypoxia is well established in many mammalian species, and is regarded as a mechanism for matching of regional perfusion to ventilation. The time course of the pulmonary vascular response to hypoxia appears to vary in different experimental settings, and few studies have examined in detail the pulmonary vascular response to isocapnic hypoxia in healthy humans. Seven healthy volunteers (2 females, 5 males) each underwent two protocols lasting 120 min. In the control protocol, they breathed through a facemask attached to a gas control system that maintained end-tidal PO2 at 100 mmHg. In the hypoxia protocol, end-tidal PO2 was maintained at 100 mmHg for 5 min but then reduced rapidly to 50 mmHg for the following 105 min, before being returned to 100 mmHg for the final 10 min. Throughout both protocols, end-tidal PCO2 was maintained 1-2 mmHg above the normal value for each participant. Participants were in the semi-left lateral position. Doppler echocardiography was used continuously to measure the maximum velocity of regurgitation across the tricuspid valve, from which the maximum systolic tricuspid valve pressure gradient (△Pmax) was calculated using Bernoulli’s equation. △Pmax was taken to be an index of pulmonary vascular tone (Dorrington & Talbot, 2004). Doppler echocardiography was also used to measure cardiac output every 5-10 min. Results were analysed using repeated measures ANOVA. Neither △Pmax nor cardiac output changed significantly during the control protocol (p>0.3, figure 1). In the hypoxia protocol, △Pmax increased significantly, compared with control (p<0.001). Two distinct components of the response were identified. Initially, △Pmax increased with a time-constant of 3.3 ± 1.5 min (mean ± SEM) and reached a plateau 6.2 ± 0.8 mmHg above the baseline. This plateau was maintained for 43.1 ± 5.1 min, before a secondary gradual increase in △Pmax began and continued throughout hypoxia. Upon returning to euoxia, △Pmax fell with a time constant of 2.1 ± 0.5 min, but did not reach baseline within 10 min. Cardiac output increased rapidly at the onset of hypoxia, decreased slightly to a nadir at ~35 min, and increased modestly throughout the rest of hypoxia. This change failed to reach statistical significance, compared with control (p>0.25). We suggest that the two distinct phases of human hypoxic pulmonary vasoconstriction we describe are likely to result from distinct underlying processes.

Where applicable, experiments conform with Society ethical requirements