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

Saturday, April 5, 2008

increase in plasma norepinephrine (NE), is a salient feature in congestive heart failure

http://content.onlinejacc.org/cgi/content/full/42/3/549

http://content.onlinejacc.org/cgi/content/full/42/3/549

Activation of the sympathetic nervous system, manifested by an increase in plasma norepinephrine (NE), is a salient feature in congestive heart failure.


J Am Coll Cardiol, 2003; 42:549-551, doi:10.1016/S0735-1097(03)00643-0
© 2003 by the American College of Cardiology Foundation

Chang-seng Liang, MD, PhD, FACC*,*

* Department of Medicine (Cardiology Unit), University of Rochester Medical Center, Rochester, New York, USA


High plasma norepinephrine and depression!

Copyright © 1999 Society of Biological Psychiatry. Published by Elsevier Science Inc.

Plasma norepinephrine and prediction of outcome in major depressive disorder

Timothy G. Johnstona, Christopher B. KellyCorresponding Author Contact Information, a, Michael R. Stevensonb and Stephen J. Coopera
a Department of Mental Health, Whitla Medical Building, The Queen’s University of Belfast, Belfast, UK (TGJ, CBK, SJC)
b Department of Medical Statistics, Mulhouse Building, The Queen’s Unversity of Belfast, Belfast, UK (MRS)
Received 1 February 1999; revised 17 May 1999; accepted 21 May 1999. Available online 30 November 1999.

Background: Several epidemiologic and clinical factors have been shown to predict long term outcome in major depressive disorder (MDD). The value of biological predictors has not been extensively studied. This study examined whether plasma norepinephrine may be useful in predicting outcome in MDD.

Methods: Forty patients were followed up 8 years after an index major depressive episode. Three outcome variables were assessed: time to first recurrence (the primary outcome measure), the Lee and Murray criteria and the Depression Outcome Scale (DOS). The results were examined against plasma norepinephrine value, at the index episode, using survival analysis and linear regression.

Results: High plasma norepinephrine at the index episode was positively and significantly associated with time to first recurrence for patients with nonpsychotic MDD (n = 31, χ2 = 8.38, on 1 df, p < .01). Similarly, plasma norepinephrine was significantly associated with good global outcome, both using Lee and Murray criteria (n = 34, adjusted R2 = .24, p < .01) and DOS criteria (n = 31, adjusted R2 = .17, p < .01) for this group of patients. In contrast, plasma norepinephrine was not significantly related to outcome for MDD with psychotic features.

Conclusions: Plasma norepinephrine at index episode seems to be a predictor of outcome in MDD.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T4S-3Y0RJKC-F&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=a88b42c007e4dcb51054a00cf6662e2d

morphological change resulting from degeneration activation

J. R. Garrett1, 2 Contact Information and A. Thulin1, 2

(1) Department of Oral Pathology, King's College Hospital Dental School, London, England
(2) Institute of Physiology, University of Lund, Lund, Sweden
(3) King's College Hospital Dental School, SE5 8RX London, England

Received: 20 May 1975

Summary Parotid glands of rat have been examined 12, 24 and 48 hours after avulsion of the cervical sympathetic ganglion and compared with the normally innervated left glands. Formaldehyde-induced fluorescence showed a relatively normal complement of adrenergic nerves at 12 hours but most of the nerves had lost their noradrenaline content by 24 hours and no fluorescent nerves were detected at 48 hours. Ultrastructural degenerative changes in axons were rare at 12 hours, common at 24 hours, and the degenerating axons appeared to have disappeared by 48 hours. The glands looked whitish and pale and similar to the controls at 12 and 48 hours but were pinkish and oedematous on the sympathectomised side at 24 hours. Correspondingly the acini were loaded with secretory granules at 12 and 48 hours but were extensively depleted of granules at 24 hours. This loss of granules is considered to be due to sympathetic ldquodegeneration secretionrdquo caused by the release of noradrenaline from the degenerating adrenergic nerves between 12 and 24 hours after ganglionectomy. This is thought to be the first example of morphological change resulting from ldquodegeneration activationrdquo to be recorded microscopically.

http://www.springerlink.com/content/n08314p052546477/

Sympathetic Hyperactivity in Chronic Renal Failure: A Wake-up Call

Sympathetic Hyperactivity in Chronic Renal Failure: A Wake-up Call

Hein A. Koomans, Peter J. Blankestijn and Jaap A. Joles

Department of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands

Correspondence to Dr. Hein A. Koomans, Department of Nephrology and Hypertension, University Medical Center Utrecht, Room F03.223, P.O. Box 85500, 3508 GA Utrecht, The Netherlands. Phone: 31-30-2507329; Fax: 31-30-2543492; E-mail: H.A.Koomans@azu.nl

ABSTRACT. Sympathetic hyperactivity plays an important and distinct role in hypertension associated with chronic renal failure (CRF). Renal ischemia, elevated angiotensin II, and suppressed brain nitric oxide (NO) all stimulate sympathetic activity. Evidence is accumulating for a role of sympathetic hyperactivity in renal and cardiac damage in patients with CRF.

Carotid distensibility, baroreflex sensitivity, and orthostatic stress

J Appl Physiol 99: 64-70, 2005. First published February 24, 2005; doi:10.1152/japplphysiol.01248.2004
8750-7587/05 $8.00

Carotid distensibility, baroreflex sensitivity, and orthostatic stress

Craig D. Steinback,1 Deborah D. O’Leary,2 Jason Bakker,1 Angela D. Cechetto,1 Hanif M. Ladak,3,4,6 and J. Kevin Shoemaker1,5

1Neurovascular Research Laboratory, School of Kinesiology, University of Western Ontario, London, Ontario; 2Department of Community Health Sciences, Brock University, St. Catharines, Ontario; Departments of 3Medical Biophysics, 4Electrical & Computer Engineering, and 5Physiology and Pharmacology, University of Western Ontario, London, Ontario; and 6Imaging Research Laboratories, Robarts Research Institute, London, Ontario, Canada

Submitted 5 November 2004 ; accepted in final form 22 February 2005

In this study, we tested the hypothesis that carotid arteries undergo rapid changes in distensibility on moving from the supine to head-up tilt (HUT) postures and, subsequently, that this change in carotid distensibility (cDa) might be associated with concurrent reductions in cardiovagal baroreflex sensitivity (BRS). Thus the effect of posture on carotid vascular mechanics and cardiovagal BRS with consideration for altered central hemodynamics (i.e., stroke volume; Doppler ultrasound) was examined. Carotid pulse pressure (cPP; Millar transducer) and contralateral B-mode ultrasound images were assessed at the carotid artery during supine and 60° HUT postures. From these measures, cDa was calculated at 5-mmHg pressure increments experienced during the cardiac cycle (n = 6). cPP (n = 9) was not different in the two postures. A smaller stroke volume being ejected into a smaller carotid artery in HUT explained the maintenance of cPP in HUT. Also, compared with supine, cDa was reset to a lower level in HUT (main effect of posture; P <> BRS (sequence method) was diminished in HUT vs. supine (P < 0.05). A positive correlation was observed between the tilt-induced changes in maximal cDa (in early systole) and cardiovagal BRS (r2 = 0.75; P <> between changes in cPP, systolic vessel dimensions, or average cDa and the corresponding change in BRS. The present results indicate that HUT elicits rapid changes in carotid artery mechanics and further suggest that reductions in the maximal cDa measured in early systole contribute to reduced cardiovagal BRS with HUT.

Patients with a history of sympathectomy were also excluded.

J Korean Acad Rehabil Med. 2000 Apr;24(2):193-199. Korean.


Comparison of Catecholamine Levels in Hemiplegic Patients with and without Reflex Sympathetic Dystrophy.

Kim EG, Kim YG, Byun SJ, Kim HS, Ahn KH.

Department of Rehabilitation Medicine, Kyung Hee University College of Medicine.
Department of Rehabilitation Medicine, Joongmoon College of Medicine.
Department of Neurology, Kyung Hee University College of Medicine.

OBJECTIVE: To determine whether the cause of sympathetic dysfunction is due to increased regional sympathetic outflow or receptor supersensitivity to circulating catecholamines in the pathogenesis of reflex sympathetic dystrophy in hemiplegia. METHOD: Ten hemiplegic patients with reflex sympathetic dystrophy were instructed to refrain from smoking or using caffeine and alcohol, and medications that influence catecholamine metabolism were witheld for 24 hours before blood sampling. Patients with cardiovascular disease, diabetes or abnormal liver and renal function tests were excluded from the study. Patients with a history of sympathectomy were also excluded.

Serum Dopamine-beta-Hydroxylase: Decrease after Chemical Sympathectomy

Serum Dopamine-beta-Hydroxylase: Decrease after Chemical Sympathectomy

Weinshilboum and Axelrod
Science 3 September 1971: 931-934
DOI: 10.1126/science.173.4000.931

Partial cardiac sympathetic denervation after bilateral thoracic sympathectomy in humans

Partial cardiac sympathetic denervation after bilateral thoracic sympathectomy in humans

Jeffrey P. Moak MDa, Basil Eldadah MD, PhDb, Courtney Holmes CMTb, Sandra Pechnik RNb and David S. Goldstein MD, PhDb
aChildren’s National Medical Center, Washington, DC
bClinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland
Received 6 January 2005; accepted 1 March 2005. Available online 25 May 2005.http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B7GW9-4G7WHD3-6&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=fd8be4ed02dd6654028265ed316ed13f

Severe bronchospasm after sympathectomy

Does bilateral thoracic sympathectomy predispose to reflex bronchospasm following tracheal intubation?

Ahed Zeidan, MD*, Nazih Nahle, MD* and Anis Baraka, MD FRCA{dagger}

* Sahel General Hospital,
{dagger} American University of Beirut Medical Center, Beirut, Lebanon,

To the Editor:

Thoracic endoscopic sympathectomy has become the technique of choice for treating intractable essential hyperhidrosis.1 We report severe bronchospasm following tracheal intubation in a patient with a previous history of bilateral thoracic sympathectomy.

Canadian Journal of Anesthesia 52:997-998 (2005)
© Canadian Anesthesiologists' Society, 2005


High Plasma Norephrine - future RENAL injury

HIGH PLASMA NOREPINEPHRINE LEVELS DETERMINED BY .BETA.2-ADRENOCEPTOR POLYMORPHISMS PREDICT THE FUTURE RENAL INJURY IN NONOBESE, NORMOTENSIVE SUBJECTS


Title;HIGH PLASMA NOREPINEPHRINE LEVELS DETERMINED BY .BETA.2-ADRENOCEPTOR POLYMORPHISMS PREDICT THE FUTURE RENAL INJURY IN NONOBESE, NORMOTENSIVE SUBJECTS
Author;MASUO KAZUKO(Baker Heart Res. Inst., Aus) MASUO KAZUKO(Osaka Univ. Graduate School Of Medicine, Jpn) KATSUYA TOMOHIRO(Osaka Univ. Graduate School Of Medicine, Jpn) KAWAGUCHI HIDEKI(Ucla, Usa) RAKUGI HIROMI(Osaka Univ. Graduate School Of Medicine, Jpn) OGIHARA TOSHIO(Osaka Univ. Graduate School Of Medicine, Jpn) TUCK MICHAEL L.(Ucla, Usa)
Journal Title;Abstr 21st Sci Meet Int Soc Hypertens 2006
Journal Code:K20060131