During Thoracoscopic sympathectomy hypotension occurs frequently.

Background : During Thoracoscopic sympathectomy hypotension occurs frequently. In this study we compared propofol with etomidate as a main anesthetic agent for thoracoscopic sympathectomy by observing intraoperative vital signs, postoperative
recovery
and side effects.
Methods : Thirty adult patients scheduled for both thoracoscopic sympathectomy were allocated to groups P (propofol) or E (etomidate). P-deletion test (PDT) was dome and plasma cortisol level was measured. In group P (n = 16), anesthesia was
induced
with fentanyl 100 μg, propofol target controlled infusion (TCI) and vecuronium. Anesthesia was maintained with N2O (60%)-propofol. MAP, HR and bispectral index were measure before induction, right after positioning, at the beginning of
right
and left sympathectomy. In group E(n = 14), anesthesia was induced and maintained with etomidate instead of propofol. Postoperative recovery was assessed on the basis of modified Aldrete scoring system at 5, 15, 30, 60 minutes postoperatively. PDT
was
performed at 1, 2 hours postoperatively. Plasma cortisol level was measured 2 h and 3 days after operation. Occurrence of myoclonic movement and nausea was recorded.
Results : MAP was lover in group P (P < 0.05). There was no difference between groups in HR, plasma cortisol concentration. The values of BIS, PDT, recovery score of group P were higher than those of group E (P< 0.05). The incidence of nausea was significantly higher in group E (P < 0.05). Conclusions : Etomidate anesthesia provided more stable vital signs during thoracoscopic sympathectomy compared to propofol anesthesia. However, in terms of recovery and nausea, better outcome was suggested in propofol anesthesia.

http://kmbase.medric.or.kr/Main.aspx?d=KMBASE&m=VIEW&i=0858220000040040262

Sympathetic regulation of Autoimmune Disease

In animal models of human autoimmune disease, alterations in sympathetic innervation, NE concentration and lymphocyte AR expression have been demonstrated. ....reduced splenic noradrenergic innervation and decreased splenic NE concentration were apparent before the onset os disease symptoms. In myelin basic protein-induced EAE and MS-like disease, a reduction in splenic NE concentration was reported at the time of maximal antigen-induced lymphocyte proliferation and was accompanied by an increase in the density of of splenic lymphocyte beta-AR. In chronic/relapsing EAE (CREAE) induced in rats, splenocyte beta-AR density correlated positively with the severity of CREAE. Removal of noradrenergic innervation by chemical sympathectomy with 6-OHDA enhanced the severity of symptoms in EAE...

Neuropsychiatry

By Randolph B. Schiffer, Stephen M. Rao, Barry S. Fogel
Published 2003
Lippincott Williams
& Wilkins

Alterations in autonomic activity have been reported in RA and MS

Neuropsychiatry

By Randolph B. Schiffer, Stephen M. Rao, Barry S. Fogel

The SNS may elicit different, and often opposing functions at different anatomic sites. Localized denervation of draining lymph nodes, with sparing of the nerves innervating the joint, exacerbated joint pathology, but sympathetic removal of sympathetic input, either by beta-AR blockade or chemical sympathectomy with 6-OHDA or guanethidine reduced arthritic symptoms. These results suggest that noradrenergic innervation of draining lymph nodes inhibits the generation of antigen-specific T cells but promotes inflammation of the joints. A similar complexity was demonstrated after beta-agonist administration. Administration of a high dose of EPI reduced the severity of experimental arthritis by an alpha2-AR-mediated mechanism, but a low dose of EPI exacerbated joint injury. These results indicate that care must be used in manipulating the SNS therapeutically in complex diseases.
The SNS may also influence autoimmune processes in humans. Alterations in autonomic activity have been reported in RA and MS, but it is not known whether these changes are induced in response to disease or whether alterations in the SNS play a role in initiating the disease. In children with juvenile RA, increased sympathetic activity and autonomic hyporesponsiveness were associated with disease exacerbation.

Published 2003
Lippincott Williams
& Wilkins

a possible mechanism for sympathectomy-induced adrenal hypertrophy

Journal of Hypertension. 17(7):933-940, July 1999.
Qiua, Jingxin 1; Nelsona, Sharon H. 1; Spethb, Robert C. 2; Wanga, Donna H. 1,3

Abstract:
Objective: Previous studies indicate that the adrenal gland plays a compensatory role in the maintenance of blood pressure in chemically sympathectomized rats. However, the mechanisms responsible for compensatory adrenal responses are poorly understood. This study examined the regulation of adrenal growth and type 1A, 1B, and type 2 angiotensin II (Ang II) receptor (AT1A, AT1B and AT2) expression in the adrenal gland induced by sympathectomy.

Methods: Five-week-old male Sprague-Dawley rats were treated with either guanethidine (50 mg/kg per day, intraperitoneally) or vehicle for 5 weeks. Norepinephrine and epinephrine levels in the atrium of the heart were measured by high-pressure liquid chromatography. Plasma renin activity was determined by radioimmunoassay. Adrenal AT1 and AT2 receptor density was determined by radioligand binding assay. Adrenal AT1A, AT1B and AT2 mRNA levels were determined by Northern blot analysis.

Results: Norepinephrine and epinephrine levels in the atrium of the heart were decreased 86% (P <>0.05), were increased in guanethidine-treated rats compared with vehicle (P < r =" 0.9," r =" 0.6," r =" 20.01,"> 0.05) expression.

Conclusions: Impairment of the sympathetic nervous system with guanethidine withdraws the normal stimulation of this system on the circulating renin-angiotensin system, but upregulates the expression of adrenal Ang II receptors. Increased expression of adrenal AT2 and AT1A receptors may play an important role in adaptive adrenal hypertrophy and hormonal responses to sympathectomy.