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dc.contributor.authorDixon, Dani Louise
dc.contributor.authorMayne, George C
dc.contributor.authorGriggs, Kim Marie
dc.contributor.authorDe Pasquale, Carmine Gerardo
dc.contributor.authorBersten, Andrew David
dc.date.accessioned2013-08-07T04:31:00Z
dc.date.available2013-08-07T04:31:00Z
dc.date.issued2012-12-17
dc.identifier.citationDixon, D.-L., Mayne, G.C., Griggs, K.M., De Pasquale, C.G. and Bersten, A.D., 2012. Chronic elevation of pulmonary microvascular pressure in chronic heart failure reduces bi-directional pulmonary fluid flux. European Journal of Heart Failure, 15(4), 368-375.en
dc.identifier.issn1388-9842
dc.identifier.urihttp://hdl.handle.net/2328/26913
dc.description.abstractAims. Chronic heart failure leads to pulmonary vascular remodelling and thickening of the alveolar–capillary barrier. We examined whether this protective effect may slow resolution of pulmonary oedema consistent with decreased bi-directional fluid flux. Methods and results. Seven weeks following left coronary artery ligation, we measured both fluid flux during an acute rise in left atrial pressure (n = 29) and intrinsic alveolar fluid clearance (n = 45) in the isolated rat lung. Chronic elevation of pulmonary microvascular pressure prevented pulmonary oedema and decreased lung compliance when left atrial pressure was raised to 20 cmH2O, and was associated with reduced expression of endothelial aquaporin 1 (P = 0.03). However, no other changes were found in mediators of fluid flux or cellular fluid channels. In isolated rat lungs, chronic LV dysfunction (LV end-diastolic pressure and infarct circumference) was also inversely related to alveolar fluid clearance (P ≤ 0.001). The rate of pulmonary oedema reabsorption was estimated by plasma volume expansion in eight patients with a previous clinical history of chronic heart failure and eight without, who presented with acute pulmonary oedema. Plasma volume expansion was reduced at 24 h in those with chronic heart failure (P = 0.03). Conclusions. Chronic elevation of pulmonary microvascular pressure in CHF leads to decreased intrinsic bi-directional fluid flux at the alveolar–capillary barrier. This adaptive response defends against alveolar flooding, but may delay resolution of alveolar oedema.en
dc.description.sponsorshipA National Health and Medical Research Council (NHMRC) grant (#375129); Australian and New Zealand College of Anaesthetists (ANZCA) grant (#08/020); the Flinders Medical Centre Foundation.en
dc.language.isoen
dc.publisherOxford University Pressen
dc.relationhttp://purl.org/au-research/grants/nhmrc/375129en
dc.rightsPublished on behalf of the European Society for Cardiology. All rights reserved. For permissions, please email journals.permissions@oup.comen
dc.subjectCritical careen
dc.subjectChronic heart failureen
dc.titleChronic elevation of pulmonary microvascular pressure in chronic heart failure reduces bi-directional pulmonary fluid fluxen
dc.typeArticleen
dc.relation.grantnumberNHMRC/375129en
dc.identifier.doihttps://doi.org/10.1093/eurjhf/hfs201en
dc.rights.holderAuthors retain copyright.en
local.contributor.authorOrcidLookupDixon, Dani Louise: https://orcid.org/0000-0001-6459-1856en_US


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