Published ahead of print on June 23, 2005, doi:10.1164/rccm.200505-699OC Am. J. Respir. Crit. Care Med., Volume 172, Number 8, October 2005, 1047-1054 A more recent version of this article appeared on October 15, 2005
Submitted on May 4, 2005 Sustained Hypoxia Depresses Sensory Processing of Respiratory Resistive LoadsDanny J Eckert1*,1 Repatriation General Hospital, Adelaide Institute for Sleep Health, Daw Park, South Australia, Australia; Discipline of Physiology, University of Adelaide, School of Molecular and Biomedical Science, Adelaide, South Australia, Australia, 2 Repatriation General Hospital, Adelaide Institute for Sleep Health, Daw Park, South Australia, Australia, 3 Musculoskeletal Research Centre, La Trobe University, Bundoora, Victoria, Australia, 4 Repatriation General Hospital, Adelaide Institute for Sleep Health, Daw Park, South Australia, Australia; Department of Medicine, Flinders University, Bedford Park, South Australia, Australia, 5 Repatriation General Hospital, Adelaide Institute for Sleep Health, Daw Park, South Australia, Australia; Discipline of Physiology, University of Adelaide, School of Molecular and Biomedical Science, Adelaide, South Australia, Australia; Department of Medicine, Flinders University, Bedford Park, South Australia, Australia * To whom correspondence should be addressed. E-mail: danny.eckert{at}rgh.sa.gov.au.
Rationale: The combination of acute hypoxia and increased respiratory load is encountered in several respiratory diseases including acute life threatening asthma and sleep apnea. Hypoxia has been shown to inhibit respiratory load perception in healthy and asthmatic subjects, and could contribute to treatment delays and impaired function of protective reflexes. Objectives: Using respiratory related evoked potentials (RREPs) this study aimed to determine the sensory processes mediating hypoxia-induced suppression of respiratory load sensation. Methods: EEG was measured over the central and parietal cortical regions in 14-healthy subjects. RREPs were elicited by 500ms mid-inspiratory resistive load stimuli during and following isocapnic normoxia or hypoxia (blood arterial O2 saturation~80%). On a separate occasion, subjects rated the perceived magnitude of 5 externally applied inspiratory resistive loads (range 8.6-43.7cmH2O[[rad]]l-1[[rad]]sec) under similar experimental conditions. In both experiments subjects voluntarily ventilated ~90% above baseline to match ventilatory output between gas conditions. Results: RREP stimulus was matched between gas conditions in 11-subjects (minimum mask pressure -9.7±0.6 vs. -9.2±0.4cmH2O). P1 and P2 amplitudes were reduced during isocapnic hypoxia compared with normoxia (maximal at Cz: P1; 2.5±1.1 vs. 3.9±1.2µv, p=0.03 and P2; 10.0±2.2 vs. 12.4±2.1µv, p<0.01 respectively). Perceived magnitude of externally applied resistive loads was also reduced during hypoxia compared to normoxia (17.1±1.1 vs. 19.0±1.1au, p<0.01). Conclusions: These data confirm that isocapnic hypoxia suppresses respiratory load sensation. Decreased amplitude of the earlier (P1) RREP component suggests that this is mediated, at least in part, by suppression of respiratory afferent information prior to its arrival at the primary sensory cortex. Key words: Dyspnea, Sensation, Event-Related Potentials, Afferent Pathways
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