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The role of prostaglandin and antioxidant availability in recovery from forearm ischemia-reperfusion injury in humans

Carter, Sophie, Faulkner, Ashton and Rakobowchuk, Mark (2014) The role of prostaglandin and antioxidant availability in recovery from forearm ischemia-reperfusion injury in humans. Journal of Hypertension, 32 (3). pp. 339-351.

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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.

Item Type: Article
Status: Published
DOI: https://doi.org/10.1097/HJH.0000000000000033
Subjects: Q Science > QP Physiology
School/Department: School of Sport
URI: http://ray.yorksj.ac.uk/id/eprint/3420

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