Please use this identifier to cite or link to this item: http://buratest.brunel.ac.uk/handle/2438/7988
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dc.contributor.authorCarter, SE-
dc.contributor.authorFaulkner, A-
dc.contributor.authorRakobowchuk, M-
dc.date.accessioned2014-02-04T12:14:51Z-
dc.date.available2014-02-04T12:14:51Z-
dc.date.issued2014-
dc.identifier.citationJournal of Hypertension, 32(2), 339 - 351, 2014en_US
dc.identifier.issn1473-5598-
dc.identifier.urihttp://journals.lww.com/jhypertension/Fulltext/2014/02000/The_role_of_prostaglandin_and_antioxidant.20.aspxen
dc.identifier.urihttp://bura.brunel.ac.uk/handle/2438/7988-
dc.descriptionThis article is made available through the Brunel Open Access Publishing Fund. It is shared under the Creative Commons License Attribution-Noncommercial No Derivative 3.0 (CCBY NCND). Copyright @ Lippincott Williams & Wilkins.en_US
dc.description.abstractBackground: Endothelial dysfunction, manifesting as attenuated flow-mediated dilation (FMD), is clinically important. Antioxidants may prevent this dysfunction; however, the acute effects of oral administration in humans are unknown. Low flow-mediated constriction (L-FMC), a further parameter of endothelial health, is largely unstudied and the mechanisms for this response unclear. Methods: Twelve healthy participants (five women and seven men) completed three test conditions: control; antioxidant cocktail (α-lipoic acid, vitamins C and E); and prostaglandin inhibitor ingestion (ibuprofen). Ultrasound measurements of brachial artery responses were assessed throughout 5 min of forearm ischemia and 3 min after. Subsequently, an ischemia–reperfusion injury was induced by a 20-min upper arm occlusion. Further, vascular function protocols were completed at 15, 30, and 45 min of recovery. Results: Endothelial dysfunction was evident in all conditions. FMD was attenuated at 15 min after ischemia–reperfusion injury (Pre: 6.24 ± 0.58%; Post15: 0.24 ± 0.75%; mean ± SD, P < 0.05), but recovered by 45 min. Antioxidant administration did not preserve FMD compared with control (P > 0.05). The magnitude of L-FMC was augmented at 15 min (Pre: 1.44 ± 0.27%; Post15: 3.75 ± 1.73%; P < 0.05) and recovered by 45 min. Ibuprofen administration produced the largest constrictive response (Pre: −1.13 ± 1.71%; Post15: −5.57 ± 3.82%; time × condition interaction: P < 0.05). Conclusion: Results demonstrate ischemia–reperfusion injury causes endothelial dysfunction and acute oral antioxidant supplementation fails to reduce its magnitude. Our results also suggest that a lack of shear stress during occlusion combined with suppression of prostaglandin synthesis magnifies L-FMC, possibly due to augmented endothelin-1 expression.en_US
dc.description.sponsorshipSociety of Biologyen_US
dc.languageeng-
dc.language.isoenen_US
dc.publisherLippincott Williams & Wilkinsen_US
dc.subjectAllometric scalingen_US
dc.subjectAntioxidantsen_US
dc.subjectFlow-mediated dilationen_US
dc.subjectIbuprofinen_US
dc.subjectLow flow-mediated constrictionen_US
dc.subjectShear rateen_US
dc.titleThe role of prostaglandin and antioxidant availability in recovery from forearm ischemia-reperfusion injury in humansen_US
dc.typeArticleen_US
dc.identifier.doihttp://dx.doi.org/10.1097/HJH.0000000000000033-
pubs.organisational-data/Brunel-
pubs.organisational-data/Brunel/Brunel Active Staff-
pubs.organisational-data/Brunel/Brunel Active Staff/School of Sport & Education-
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Brunel OA Publishing Fund
Dept of Life Sciences Research Papers

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