Show simple item record

dc.contributor.authorCoppel, Jonny
dc.contributor.authorGilbert-Kawai, E
dc.contributor.authorBottomley, T
dc.contributor.authorSugarman, J
dc.contributor.authorMartin, Daniel
dc.date.accessioned2020-09-20T11:13:59Z
dc.date.issued2019-12
dc.identifier.issn0049-3848
dc.identifier.issn1879-2472
dc.identifier.urihttp://hdl.handle.net/10026.1/16400
dc.description.abstract

INTRODUCTION: The physiological impact of hypoxia on coagulation has significant importance in the clinical setting, but it is not yet fully understood. Various static methods exist to investigate the process of coagulation, however, thromboelastography (TEG) provides a dynamic assessment of clot formation that can be quantitatively assessed. METHOD: Twenty-five participants were exposed to normobaric hypoxia (12.5% oxygen) for 8 h. Venous blood was taken from the participants directly pre- and post-hypoxic exposure, and coagulation was tested using TEG. Coagulation variables assessed included reaction time, split point, alpha angle, kinetics and maximum amplitude. RESULTS: Time taken for clot initiation, (assessed using the split point and reaction time) was significantly reduced after 8 h of hypoxic exposure. The split point reduced from a mean of 5.20 to 4.23 min (p = 0.022), whilst the reaction time reduced from 6.09 to 4.94 min (p = 0.004). Maximum amplitude, alpha angle and kinetics did not change significantly after hypoxic exposure. CONCLUSION: The results demonstrate that subacute normobaric hypoxic exposure increases the tendency for whole blood to coagulate, as demonstrated by a reduced split and reaction time using TEG.

dc.format.extent105-109
dc.format.mediumPrint-Electronic
dc.languageen
dc.language.isoeng
dc.publisherElsevier BV
dc.subjectHypoxia
dc.subjectThromboelastography
dc.subjectHaemostasis
dc.titleThe effect of normobaric hypoxic exposure on coagulation as measured by thromboelastography
dc.typejournal-article
dc.typeJournal Article
plymouth.author-urlhttps://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000497807900017&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=11bb513d99f797142bcfeffcc58ea008
plymouth.volume184
plymouth.publication-statusPublished
plymouth.journalThrombosis Research
dc.identifier.doi10.1016/j.thromres.2019.10.032
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/Peninsula Medical School
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
dc.publisher.placeUnited States
dcterms.dateAccepted2019-10-31
dc.rights.embargodate9999-12-31
dc.identifier.eissn1879-2472
dc.rights.embargoperiodNot known
rioxxterms.versionofrecord10.1016/j.thromres.2019.10.032
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2019-12
rioxxterms.typeJournal Article/Review


Files in this item

Thumbnail
Thumbnail

This item appears in the following Collection(s)

Show simple item record


All items in PEARL are protected by copyright law.
Author manuscripts deposited to comply with open access mandates are made available in accordance with publisher policies. Please cite only the published version using the details provided on the item record or document. In the absence of an open licence (e.g. Creative Commons), permissions for further reuse of content should be sought from the publisher or author.
Theme by 
Atmire NV