PARTIAL PULMONARY SYMPATHETIC DENERVATION BY THORACOSCOPIC D2-D3 SYMPATHICOLYSIS FOR ESSENTIAL HYPERHIDROSIS - EFFECT ON THE PULMONARY DIFFUSION CAPACITY

In patients with essential hyperhidrosis (EH), a pathological conditio n characterized by increased activity of the upper dorsal sympathetic ganglia D-2-D-3, anatomical interruption at the D-2-D-3 level by thora coscopic sympathicolysis (TS) is a safe and effective treatment. The D -2 and D-3 ganglia, however, are also in the pathway of sympathetic lu ng innervation, which may influence the pulmonary diffusion capacity f or carbon monoxide (expressed as transfer factor for CO:TLCO, and as t ransfer coefficient for CO:KCO). We therefore studied the effect of TS on TLCO and KCO in 50 EH patients: compared with pre-operative values , both TLCO (-6.7%, P<0.001) and KCO (-4.2%, P=0.002) were significant ly decreased at 6 weeks after bilateral TS, an effect which was indepe ndent of the smoking status of the patients. In order to explain this phenomenon, the following pharmacological interventions were studied: (1) oral beta(1+2)-adrenoreceptor blockade with propranolol caused a c omparable decrease of TLCO (-6.3%) and KCO (-7.5%) in matched normal s ubjects, but had no effect on TLCO and KCO in EH patients prior to TS; and (2) subsequent inhalation of the beta(2)-adrenoreceptor agonist s albutamol in a dosage suspected to cause alveolar beta-receptor stimul ation had no effect on TLCO and KCO, neither in the normal subjects, n or in EH patients (before and after TS). Although the exact mechanism of the TS-induced decrease in TLCO and KCO remains speculative, these findings suggest that they may be related to a beta(1)-adrenoreceptor- mediated change in pulmonary capillary membrane permeability, although TS-induced changes in pulmonary blood flow or an interplay of both me chanisms cannot be excluded.