dc.contributor.author |
Burrowes, Kelly |
en |
dc.contributor.author |
Clark, Alys |
en |
dc.contributor.author |
Wilsher, ML |
en |
dc.contributor.author |
Milne, DG |
en |
dc.contributor.author |
Tawhai, Merryn |
en |
dc.date.accessioned |
2016-11-14T03:18:02Z |
en |
dc.date.issued |
2014-08 |
en |
dc.identifier.citation |
Annals of Biomedical Engineering 42(8):1631-1643 Aug 2014 |
en |
dc.identifier.issn |
0090-6964 |
en |
dc.identifier.uri |
http://hdl.handle.net/2292/31025 |
en |
dc.description.abstract |
Hypoxic pulmonary vasoconstriction (HPV) is an adaptive response unique to the lung whereby blood flow is diverted away from areas of low alveolar oxygen to improve ventilation-perfusion matching and resultant gas exchange. Some previous experimental studies have suggested that the HPV response to hypoxia is blunted in acute pulmonary embolism (APE), while others have concluded that HPV contributes to elevated pulmonary blood pressures in APE. To understand these contradictory observations, we have used a structure-based computational model of integrated lung function in 10 subjects to study the impact of HPV on pulmonary hemodynamics and gas exchange in the presence of regional arterial occlusion. The integrated model includes an experimentally-derived model for HPV. Its function is validated against measurements of pulmonary vascular resistance in normal subjects at four levels of inspired oxygen. Our results show that the apparently disparate observations of previous studies can be explained within a single model: the model predicts that HPV increases mean pulmonary artery pressure in APE (by 8.2 ± 7.0% in these subjects), and concurrently shows a reduction in response to hypoxia in the subjects who have high levels of occlusion and therefore maximal HPV in normoxia. |
en |
dc.format.medium |
Print-Electronic |
en |
dc.language |
eng |
en |
dc.publisher |
Springer Verlag (Germany) |
en |
dc.relation.ispartofseries |
Annals of Biomedical Engineering |
en |
dc.rights |
Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. Details obtained from http://www.sherpa.ac.uk/romeo/issn/0090-6964/ |
en |
dc.rights.uri |
https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm |
en |
dc.subject |
Pulmonary Artery |
en |
dc.subject |
Animals |
en |
dc.subject |
Dogs |
en |
dc.subject |
Humans |
en |
dc.subject |
Pulmonary Embolism |
en |
dc.subject |
Anoxia |
en |
dc.subject |
Pulmonary Gas Exchange |
en |
dc.subject |
Vascular Resistance |
en |
dc.subject |
Pulmonary Circulation |
en |
dc.subject |
Vasoconstriction |
en |
dc.subject |
Models, Biological |
en |
dc.subject |
Adult |
en |
dc.subject |
Middle Aged |
en |
dc.subject |
Female |
en |
dc.subject |
Male |
en |
dc.subject |
Arterial Pressure |
en |
dc.title |
Hypoxic pulmonary vasoconstriction as a contributor to response in acute pulmonary embolism |
en |
dc.type |
Journal Article |
en |
dc.identifier.doi |
10.1007/s10439-014-1011-y |
en |
pubs.issue |
8 |
en |
pubs.begin-page |
1631 |
en |
pubs.volume |
42 |
en |
dc.description.version |
AM - Accepted Manuscript |
en |
dc.identifier.pmid |
24770844 |
en |
pubs.end-page |
1643 |
en |
dc.rights.accessrights |
http://purl.org/eprint/accessRights/OpenAccess |
en |
pubs.subtype |
Article |
en |
pubs.elements-id |
444292 |
en |
pubs.org-id |
Bioengineering Institute |
en |
pubs.org-id |
ABI Associates |
en |
dc.identifier.eissn |
1573-9686 |
en |
pubs.record-created-at-source-date |
2016-11-14 |
en |
pubs.dimensions-id |
24770844 |
en |