A corticosteroid, a non-steroidal anti-inflammatory drug and an antihistamine modulate in vivo vascular reactions before and during post-occlusive hyperaemia

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Abstract
Post-occlusive reactive hyperaemia is the temporary increase of blood flow in a tissue following transient vascular obstruction, and has recently heen proposed as an in vivo method for ranking topical corticosteroid potency. We investigated in vivo vascular reactions before and during postocclusive hyperaemia using laser-Doppler flowmetry and reflectance spectroscopy (RS). RS enables resolution of in vivo erythema into deoxygenated (venous) [DOH] and oxygenated (arterial) haemoglobin (OH) components (expressed in arbitrary units. All). Using a randomized 24-h occlusive exposure in 10 healthy volunteers the effects of a corticosteroid (betamethasone-1 7-valerate). a non-steroidal anti-inflammatory drug (NSAID) [indomethacin], an antihistamine (diphenydramine), or vehicle, were studied before and during post-occlusive hyperaemia. The 24-h vehicle exposure decreased total haemoglobin (composed of a small increase in OH [PPPPPPP005). Diphenhydramine caused no significant changes in RS or laser-Doppler flowmetry readings hefore post-occlusive hyperaemia. Post-occlusive hyperaemia increased total haemoglobin maximally at the first observation time (OH. 0.63±0.13 AU: DOH. 0.31±0.11 AU [P<0.001]). OH increased (178%) maximally at 30 s (OH. 0.64±0.16 AU). and DOH was decreased throughout the observation period. The blood flow in vehicle-exposed sites increased 193%. also with a maximal increase at the 30-s reading. At all post-occlusive time intervals the increase in OH was significantly reduced hy hetamethasone-17-valerate. indomethacin and diphenhydramine. The greatest decrease in post-occlusive OH occurred with betamethasone-17-vaIerate. The increase in blood flow was also significantly reduced at all post-occlusive time intervals with betamethasone-17-valerate. Indomethacin also decreased blood flow, but this was only significant at 2 and 3 min. No significant blood flow changes were found after diphenhydramine exposure. Blanching was caused both by corticosteroid and NSAID, which suggests that vasoconstriction may be partially caused by inhibition of mediators from the arachidonic acid cycle pathway. Post-occlusive hyperaemia appeared to be partiafly induced by release of inflammatory mediators.