Please use this identifier to cite or link to this item: http://buratest.brunel.ac.uk/handle/2438/7988
Title: The role of prostaglandin and antioxidant availability in recovery from forearm ischemia-reperfusion injury in humans
Authors: Carter, SE
Faulkner, A
Rakobowchuk, M
Keywords: Allometric scaling;Antioxidants;Flow-mediated dilation;Ibuprofin;Low flow-mediated constriction;Shear rate
Issue Date: 2014
Publisher: Lippincott Williams & Wilkins
Citation: Journal of Hypertension, 32(2), 339 - 351, 2014
Abstract: Background: 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.
Description: This 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.
URI: http://journals.lww.com/jhypertension/Fulltext/2014/02000/The_role_of_prostaglandin_and_antioxidant.20.aspx
http://bura.brunel.ac.uk/handle/2438/7988
DOI: http://dx.doi.org/10.1097/HJH.0000000000000033
ISSN: 1473-5598
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Brunel OA Publishing Fund
Dept of Life Sciences Research Papers

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