Control of cutaneous blood vessels in psoriatic plaques

The aim of this study was to compare local blood flow in psoriatic plaques before and after provocations known to alter cutaneous vascular resistance, in order to determine whether plaque hyperemia is caused by a failure of n ormal vascular control mechanisms. Cutaneous blood flow was recorded using a laser Doppler flowmeter over plaque skin (plaque site) and clinically nor mal skin (nonplaque site) on the opposite am, at least 5 cm away from the n earest plaque. It is important to note that most of the laser Doppler signa l comes from the subpapillary plexus of the skin and only a small portion ( 2%-10%) is produced by capillary blood flow. In the psoriatic plaques the b asal flux was between nine and 13 times greater than nonplaque skin. The bi ologic zero (a signal independent of perfusion, which also persists after c omplete proximal arterial occlusion) was also significantly greater at plaq ue sites compared with nonplaque sites. Sympathetic and local vasoconstrict ion in psoriatic skin was shown to be intact and responses to vasodilator t ests were likewise intact, i.e., there was no failure of response to normal vascular control mechanisms, albeit some quantitative differences. Tests o f vasodilatation indicated that, although basal flux is high in plaque comp ared with nonplaque skin, arterioles supplying plaque skin can dilate furth er, i.e., lesional arterioles are not normally maximally dilated but have a basal constrictor tone. Interestingly, the red cell flux at maximum dilata tion in nonplaque skin is less than even the basal flux in plaque skin, Thi s means that in plaque skin either there are more arterioles than in nonpla que skin, or there is chronic, structural widening of the existing arteriol es in plaque skin.