Thoracoscopic sympathectomy at the T2 or T3 level facilitates bradykinin-induced protein extravasation in human forearm skin.

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.