Controlled dermal cell damage as human in vivo model for localised pain and inflammation
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Objective and Design: An unspecific human in vivo model of dermal pain and inflammation was developed by means of limited, localised and controlled cell damage.
Subjects: Twelve participants were recruited.
Treatment: Dermal microdialysis was used to deliver randomised and single blinded aqueous sodium dodecyl sulphate (SDS) at concentrations of 0.01%, 0.1% and 0.5% w/v to the volar forearm.
Methods: Nociceptive responses were recorded on a numerical scale, vasodilatation was assessed by laser Doppler scanning and sampled tissue fluid was analysed for PGE2 by ELISA.
Results: Saline control and 0.01% SDS did not differ in their ability to cause vasodilatation, flare reaction or pain. In contrast, SDS (0.1 and 0.5%) evoked a significant increase of blood flow (p<0.005), a widespread reddening (p<0.01), and stinging-burning pain (p<0.005). PGE2 concentration in the dialysate did not change during 0.01% SDS perfusion (p>0.9), but increased significantly following the stimulation with 0.1% and 0.5% SDS (20 to 30-fold). No significant differences of released PGE2 levels were determined between 0.1% and 0.5% SDS stimulation (p>0.05).
Conclusions: We demonstrated that localised intradermal administration of SDS induces a limited pain and inflammatory response in humans. Excitation of nociceptors was accompanied by a massive PGE2 release. Employing this experimental model, the relative contribution of endogenous mediators to induce, maintain or facilitate pain and vasodilatation can be investigated.
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