The amount of compensatory sweating depends on the patient, the damage that the white rami communicans incurs, and the amount of cell body reorganization in the spinal cord after surgery.
Other potential complications include inadequate resection of the ganglia, gustatory sweating, pneumothorax, cardiac dysfunction, post-operative pain, and finally Horner’s syndrome secondary to resection of the stellate ganglion.
www.ubcmj.com/pdf/ubcmj_2_1_2010_24-29.pdf

After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion undergo transneuronic degeneration
After severing the sympathetic trunk, the cells of its origin undergo complete disintegration within a year.
http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

Thursday, May 1, 2008

beta 1-adrenoreceptor-mediated change in pulmonary capillary membrane permeability

Respir Med. 1997 Oct;91(9):537-45.Click here to read Links
Partial pulmonary sympathetic denervation by thoracoscopic D2-D3 sympathicolysis for essential hyperhidrosis: effect on the pulmonary diffusion capacity.
Noppen MM, Vincken WG.

Respiratory Division, Academic Hospital, University of Brussels, Belgium.

In patients with essential hyperhidrosis (EH), a pathological condition characterized by increased activity of the upper dorsal sympathetic ganglia D2-D3, anatomical interruption at the D2-D3 level by thoracoscopic sympathicolysis (TS) is a safe and effective treatment. The D2 and D3 ganglia, however, are also in the pathway of sympathetic lung innervation, which may influence the pulmonary diffusion capacity for carbon monoxide (expressed as transfer factor for CO:TLCO, and as transfer 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 significantly decreased at 6 weeks after bilateral TS, an effect which was independent 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 comparable decrease of TLCO (-6.3%) and KCO (-7.5%) in matched normal subjects, but had no effect on TLCO and KCO in EH patients prior to TS; and (2) subsequent inhalation of the beta 2-adrenoreceptor agonist salbutamol in a dosage suspected to cause alveolar beta-receptor stimulation had no effect on TLCO and KCO, neither in the normal subjects, nor 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 mechanisms cannot be excluded.