Previously [Histochem J 1997;29:279-286], we found that sympathectomy induced neointima formation in ear but not cerebral arteries of genetically hyperlipidemic rabbits.
Sympathectomy Causes Aggravated Lesions and Dedifferentiation in Large Rabbit Atherosclerotic Arteries without Involving Nitric Oxide
J Vasc Res 2006;43:289-305 (DOI: 10.1159/000093010)
Sunday, March 29, 2009
sympathectomy severs both vasomotor and sensory fibres
Lumbar sympathectomy severs both vasomotor and sensory fibres, suggesting that relief of rest pain may be explained not only by increased cutaneous and muscle blood flow, but also by nociceptive sensory denervation.
Brendon J. Coventry* and John A. Walsh†
Brendon J. Coventry* and John A. Walsh
*Department of Surgery, University of Adelaide, Royal Adelaide Hospital and † VascularSurgery Unit, Department of Surgery, Flinders University, Flinders Medical Centre, Adelaide, South Australia, Australia
ANZ Journal of Surgery
Volume 73 Issue 1-2, Pages 14 - 18
Published Online: 5 Feb 2003
Journal compilation © 2009 Royal Australasian College of Surgeons
neuropeptide Y-like immunoreactive nerves in the dura mater after sympathectomy
These results suggest that as a consequence of long-term sympathectomy with guanethidine, compensatory changes occur, involving an increase in the expression of neuropeptide Y-like immunoreactivity in non-sympathetic axons in cerebrovascular nerves and iris of the rat. In contrast, the neuropeptide Y-like immunoreactive nerves in the dura mater appear to be entirely sympathetic, since none were present after short-term sympathectomy and none appeared after long-term sympathectomy.
Neuroscience. 1990;34(2):369-78.
PMID: 2333147 [PubMed - indexed for MEDLINE
Neuroscience. 1990;34(2):369-78.
PMID: 2333147 [PubMed - indexed for MEDLINE
sympathectomy enhances the severity of EAE
It is now well established that the immune system and the nervous system are connected bidirectionally ( 8, 9, 10 ). Although much remains to be investigated, several lines of evidence suggest that the sympathetic nervous system (SNS) provides a major pathway for neuroimmune interactions. Indeed, a role for catecholamines such as norepinephrine and epinephrine in SNS-mediated immunoregulation has been implicated in various conditions ( 11, 12, 13, 14, 15 ). Regarding the modulation of autoimmunity, it was previously demonstrated that depletion of SNS transmitters by chemical sympathectomy enhances the severity of EAE ( 11, 12 ). Because -adrenoceptor agonists protect against EAE ( 13 ) and catecholamines modulate several immunological functions critical to the pathogenesis of EAE ( 14 ), the enhancement of EAE by chemical sympathectomy has largely been attributed to the depletion of catecholamines. However, although neuropeptide Y (NPY) is also released from SNS terminals innervating lymphatic tissues ( 16, 17 ), no previous studies have explored the possibility that depletion of other SNS transmitters such as NPY may contribute to these findings.
Prior studies have revealed that the sympathetic nervous system regulates the clinical and pathological manifestations of experimental autoimmune encephalomyelitis (EAE), an autoimmune disease model mediated by Th1 T cells. Although the regulatory role of catecholamines has been indicated in the previous works, it remained possible that other sympathetic neurotransmitters like neuropeptide Y (NPY) may also be involved in the regulation of EAE.
In conclusion, this study demonstrates for the first time to our knowledge that NPY has an immunomodulatory activity that suppresses signs of EAE. Given that the levels of NPY in the CSF are reduced in patients with MS ( 34, 35 ), it is tempting to speculate that NPY may also play a critical role in preventing the development of MS. With the availability of novel and highly selective agonists and their ability to mimic the effects of NPY in a highly specific manner, we propose that targeting NPY receptors may be a promising new therapeutic approach to autoimmune disorders.
Department of Immunology, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, Japan; Department of Biochemistry, University of Leipzig, Leipzig, Germany; and Department of Functional and Applied Anatomy, Hannover Medical School, Hannover, Germany
Prior studies have revealed that the sympathetic nervous system regulates the clinical and pathological manifestations of experimental autoimmune encephalomyelitis (EAE), an autoimmune disease model mediated by Th1 T cells. Although the regulatory role of catecholamines has been indicated in the previous works, it remained possible that other sympathetic neurotransmitters like neuropeptide Y (NPY) may also be involved in the regulation of EAE.
In conclusion, this study demonstrates for the first time to our knowledge that NPY has an immunomodulatory activity that suppresses signs of EAE. Given that the levels of NPY in the CSF are reduced in patients with MS ( 34, 35 ), it is tempting to speculate that NPY may also play a critical role in preventing the development of MS. With the availability of novel and highly selective agonists and their ability to mimic the effects of NPY in a highly specific manner, we propose that targeting NPY receptors may be a promising new therapeutic approach to autoimmune disorders.
Department of Immunology, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, Japan; Department of Biochemistry, University of Leipzig, Leipzig, Germany; and Department of Functional and Applied Anatomy, Hannover Medical School, Hannover, Germany
Effects of sympathectomy on heart size and function
This evidence suggests that elimination of the adrenergic nervous system's chronotropic influence promotes greater left ventricular filling, and the resultant increase in preload may importantly contribute to the stimulation of cardiac hypertrophy.
Am J Physiol Heart Circ Physiol 252: H442-H447, 1987;
Am J Physiol Heart Circ Physiol 252: H442-H447, 1987;
Effects of chemical sympathectomy on insulin receptors and insulin action
Glucose metabolism, however, was inhibited by chemical sympathectomy: the glucose transport rate was significantly reduced and fatty acid synthesis was nearly totally abolished. Insulin was still effective in stimulating both parameters but failed to restore normal levels. The results suggest that the sympathetic innervation of adipose tissue may exert an inhibitory effect on the number of high-affinity insulin receptors as well as on the sensitivity of the lipolysis to insulin, as both parameters were increased by sympathectomy.
Volume 229, Issue 3, pp. 839-844, 06/01/1984
Volume 229, Issue 3, pp. 839-844, 06/01/1984
Copyright © 1984 by American Society for Pharmacology and Experimental Therapeutics
altering Ca2+ activity of actomyosin ATPase
Also, Sx (surgical sympathectomy) may impair cardiac functional capacity by altering Ca2+ activity of actomyosin ATPase.
Am J Physiol. 1979 Jan;236(1):C30-4.
Am J Physiol. 1979 Jan;236(1):C30-4.
PMID: 219702 [PubMed - indexed for MEDLINE]
Effect of chemical sympathectomy on serum levels of thyroid hormones and the biochemical profile
The cloacal temperature (Tc) and both the thyroid hormones showed a drastic decrease while the T3/T4 ratio was augmented as a result of sympathectomy.
Thus, the influence of SNS appears to be crucial in the maintenance of serum thyroid hormones and body temperature, as well as metabolic activities of hepatic cells.
Thus, the influence of SNS appears to be crucial in the maintenance of serum thyroid hormones and body temperature, as well as metabolic activities of hepatic cells.
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