Transient cold pain has no effect on cutaneous vasodilatation induced by capsaicin: A randomized-control-crossover study in healthy subjects

Cooling the skin induces sympathetically driven vasoconstriction, along with some vasoparalytic dilatation at lowermost temperatures. Neurogenic inflammation, on the other hand, entails vasodilatation. In the present study, we examined the dynamic vasomotor balance of capsaicin-induced vasodilatation within the area of the induced neurogenic inflammation, with and without superimposed cooling. In a randomized-control-crossover fashion, a sample of 14 healthy volunteers participated in three experiments: (1) exposure to each 0°C cold pain stimulus and a neutral 30°C stimulus (control) for 30 s to the volar forearms by contact thermal thermode (1.6×1.6 cm²), (2) injection of 50 μg intradermal capsaicin without cooling and (3) injection of capsaicin followed by application of 0°C cold pain stimulation for 30 s within the area of the secondary hyperalgesia. Repetitive vascular measurements over skin area of 4.0×4.0 cm² of blood flux (BF) were acquired before and during the 5 min after stimulation. A marked increase in BF (i.e. vasodilatation) at the location of the cold stimulus in comparison to control (30°C) (F=11.97, p=0.004) within the first 3 min was demonstrated. Two-way repeated-measures ANOVA indicated no interaction between the experimental conditions (capsaicin with or without cold) and time (F=0.934, p=0.454). The cold pain stimulation was found to be insignificant in its influence on BF evoked by capsaicin (F=0.018, p=0.894). The results of our study indicate that (1) transient cooling causes significant vasodilatation, (2) intradermal injection of capsaicin is dominant in inducing vasodilatation, and (3) the cold-pain-evoked vasodilatation has no modulative effect on the capsaicin-evoked cutaneous vasodilatation.