Why the study?
Does cyclo-oxygenase inhibition with ketoprofen alter postocclusive reactive hyperaemia in the skin of healthy volunteers?
Does cyclo-oxygenase inhibition with ketoprofen alter postocclusive reactive hyperaemia in the skin of healthy volunteers?
Cyclo-oxygenase inhibition does not alter skin postocclusive reactive hyperaemia, indicating prostanoids are not involved in this cutaneous vasodilatory response in healthy humans.
COX inhibition leaves skin PORH unchanged; challenges prostanoid mediation and leaves open primary mechanisms for microvascular testing.
Several mediators contribute to postocclusive reactive hyperaemia (PORH) in the skin, including sensory nerves and endothelium-derived hyperpolarizing factors. The main objective of this study was to investigate the specific involvement of prostanoids in human skin PORH. We tested the effect of the inhibition of cyclo-oxygenases (COX) by 4 mm ketoprofen, infused through microdialysis fibers inserted into the healthy volunteers forearm skin, following 5 min brachial artery occlusion. Skin microvascular blood flux was recorded using two-dimensional Laser Speckle Contrast Imaging. Maximal cutaneous vascular conductance (CVCmax ) was obtained following the perfusion of 29 mm sodium nitroprusside. A systematic review of the effects of COX inhibitors on skin peak PORH was also performed. We observed no significant difference between ketoprofen and placebo for the PORH peak (78 ± 8 and 71 ± 19% CVCmax , respectively) and area under the curve (2951 ± 721 and 2490 ± 936% CVCmax .s). A meta-analysis showed a substantial heterogeneity between studies, with overall a neutral effect of COX inhibition on peak PORH. Cyclo-oxygenase inhibition does not alter skin PORH, suggesting no involvement of prostanoids in cutaneous postocclusive vasodilatation in healthy humans.
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Hellmann et al. (2015) studied this question.
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