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| Research article summary (published 30 Jan 1995): |
Ventilatory response to isocapnic hyperoxia.
Full Abstract
Breathing O2 for up to 1 h has been shown to either not influence or slightly increase (6-13%) minute ventilation. However, end-tidal PCO2 was not kept constant in these experiments. In nine healthy men, we studied the ventilatory, blood pressure, and heart rate responses to 30 min of normobaric hyperoxia (50% O2) at isocapnic conditions. Hyperoxia led to a 60% increase in mean minute ventilation (P = 0.002), largely due to an increase in mean tidal volume from 0.66 +/- 0.04 (SE) to 0.88 +/- 0.05 liter (P = 0.007). Fifteen minutes after the termination of hyperoxia, minute ventilation was still increased (P = 0.02) compared with baseline, although it was reduced compared with hyperoxia (P = 0.02). Arterial blood gas analyses in six subjects before and during hyperoxia showed an increase in arterial PO2 and O2 saturation but no change in arterial PCO2 or pH. Hyperoxia induced no changes in arterial blood pressure or heart rate. We conclude that 1) isocapnic hyperoxia stimulates respiration markedly, an effect that is approximately five times higher than previously measured; 2) the increase in ventilation induced by hyperoxia does not affect arterial blood pressure and heart rate; and 3) in experiments using hyperoxia, its effect on breathing and subsequently on PCO2 has to be taken into account.
Author information
Author/s: Becker, H (H); Polo, O (O); McNamara, S G (SG); Berthon-Jones, M (M); Sullivan, C E (CE);
Affiliation: Department of Medicine, University of Sydney, New South Wales, Australia.
Journal and publication information
Publication Type: Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
Journal: Journal of applied physiology (Bethesda, Md. : 1985) (J Appl Physiol), published in UNITED STATES. (Language: eng)
Reference: 1995-Feb; vol 78 (issue 2) : pp 696-701
Dates: Created 1995/06/29; Completed 1995/06/29; Revised 2006/11/15;
PMID: 7759442, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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