Background: The endogenous peptide bradykinin (BK) is an inflammatory mediator that induces nociceptor activation and sensitization as well as protein extravasation and vasodilation.
Objective: To test the hypothesis if sympathectomy affects BK-induced inflammation in humans.
Methods: Dermal microdialysis was employed on the volar forearm in 10 patients (21-41 years) with regional hyperhidrosis before and three months after preganglionic endoscopic transthoracic sympathetic clipping (ETSC) at the T2 or T3 level and in 10 healthy volunteers (22-36 years). After 60 minutes perfusion with Ringer's solution microdialysis fibers were perfused with BK 10(-7) M and 10(-5) M for 30 minutes followed by 30 minutes Ringer's solution again. To assess protein extravasation dialysate protein content was measured photometrically and Laser-Doppler imaging was used to quantify axonreflex vasodilation.
Results: Baseline flux values after ETSC were higher as compared with controls and preoperative values (anova, Bonferroni post hoc test, P < 0.05), but neither BK 10(-7) M nor 10(-5) M led to significant vasodilation. Baseline dialysate protein did not significantly differ between groups. BK 10(-5) M induced protein extravasation while BK 10(-7) M was ineffective, and BK 10(-5) M induced protein extravasation was significantly enhanced after ETSC (P < 0.001).
Conclusions: Forearm skin perfusion is increased after ETSC on the T2 or T3 level indicating decreased sympathetic activity while BK-induced protein extravasation was increased. These results show that preganglionic sympathectomy does not diminish bradykinin-induced protein extravasation as found for postganglionic sympathectomy in rats.