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dc.contributor.authorHoiland, Ryan
dc.contributor.authorFoster, Glen
dc.contributor.authorDonnelly, Joseph
dc.contributor.authorStembridge, Mike
dc.contributor.authorWillie, Christopher
dc.contributor.authorSmith, Kurt J.
dc.contributor.authorLewis, Nia C. S.
dc.contributor.authorLucas, Samuel J.E.
dc.contributor.authorCotter, Jim D.
dc.contributor.authorYeoman, David J.
dc.contributor.authorThomas, Kate
dc.contributor.authorDay, Trevor A.
dc.contributor.authorTymko, Michael
dc.contributor.authorBurgess, Keith R.
dc.contributor.authorAinslie, Philip
dc.date.accessioned2016-11-25T14:58:05Z
dc.date.available2016-11-25T14:58:05Z
dc.date.issued2015-07
dc.identifier.citationHoiland, R.L., Foster, G.E., Donnelly, J., Stembridge, M., Willie, C.K., Smith, K.J., Lewis, N.C., Lucas, S.J., Cotter, J.D., Yeoman, D.J., Thomas, K.N., Day, T.A., Tymko, M., Burgess, K.R., Ainslie, P.N.(2015) 'Chemoreceptor responsiveness at sea level does not predict the pulmonary pressure response to high altitude', CHEST Journal, 148(1), pp.219-225.en_US
dc.identifier.issn0012-3692
dc.identifier.urihttp://hdl.handle.net/10369/8194
dc.descriptionThis article was published in Chest in July 2015, available at http://dx.doi.org/10.1378/chest.14-1992en_US
dc.description.abstractThe hypoxic ventilatory response (HVR) at sea level (SL) is moderately predictive of the change in pulmonary artery systolic pressure (PASP) to acute normobaric hypoxia. However, because of progressive changes in the chemoreflex control of breathing and acid-base balance at high altitude (HA), HVR at SL may not predict PASP at HA. We hypothesized that resting peripheral oxyhemoglobin saturation (SpO2) at HA would correlate better than HVR at SL to PASP at HA. In 20 participants at SL, we measured normobaric, isocapnic HVR (L/min·-%SpO2 -1) and resting PASP using echocardiography. Both resting SpO2 and PASP measures were repeated on day 2 (n=10), days 4-8 (n=12), and 2-3 weeks (n=8) after arrival at 5050m. These data were also collected at 5050m on life-long HA residents (Sherpa; n=21). Compared to SL, SpO2 decreased from 98.6 to 80.5% (P<0.001), while PASP increased from 21.7 to 34.0mmHg (P<0.001) after 2-3 weeks at 5050m. Isocapnic HVR at SL was not related to SpO2 or PASP at any time point at 5050m (all P>0.05). Sherpa had lower PASP (P<0.01) than lowlanders on days 4-8 despite similar SpO2. Upon correction for hematocrit, Sherpa PASP was not different from lowlanders at SL, but lower than lowlanders at all HA time points. At 5050m, whilst SpO2 was not related to PASP in lowlanders at any point (all R2=<0.05; P>0.50), there was a weak relationship in the Sherpa (R2=0.16; P=0.07). We conclude that neither HVR at SL nor resting SpO2 at HA correlates with elevations in PASP at HA.en_US
dc.language.isoenen_US
dc.publisherElsevieren_US
dc.relation.ispartofseriesChest;
dc.titleChemoreceptor responsiveness at sea level does not predict the pulmonary pressure response to high altitudeen_US
dc.typeArticleen_US
dc.identifier.doihttp://dx.doi.org/10.1378/chest.14-1992
dcterms.dateAccepted2014-11-13
rioxxterms.funderCardiff Metropolitan Universityen_US
rioxxterms.identifier.projectCardiff Metropolian (Internal)en_US
rioxxterms.versionAMen_US
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by-nc-nd/3.0/en_US
rioxxterms.licenseref.startdate2016-11-25
rioxxterms.funder.project37baf166-7129-4cd4-b6a1-507454d1372een_US


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