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Partial peripheral neuropathy and denervation induced adrenoceptor supersensitivity. Functional studies in an
1Department of Surgery, University Hospital Maastricht, The Netherlands.
Acta Orthopaedica Belgica
|May 20, 1998
Summary
Neuropathic pain in rats involves sympathetic dysfunction. This study found increased sensitivity to catecholamines in arteries from ligated sciatic nerves, indicating denervation supersensitivity.
Area of Science:
- Neuroscience
- Physiology
- Pharmacology
Background:
- Chronic constriction injury (CCI) in rats models neuropathic pain, including reflex sympathetic dystrophy (RSD).
- Sympathetic dysfunction, potentially due to denervation-induced supersensitivity to catecholamines, is implicated in CCI and RSD.
Purpose of the Study:
- To investigate the functional properties of sympathetic innervation in rat hind paw subcutaneous resistance arteries following sciatic nerve ligation (CCI).
- To determine if sympathetic dysfunction in this neuropathic pain model involves altered nerve responsiveness or receptor sensitivity.
Main Methods:
- Subcutaneous resistance arteries were isolated from the hind paws of rats 3 weeks after CCI.
- Contractile responses were measured using a myograph during electric field stimulation of adrenergic nerves and administration of adrenergic agonists.
Main Results:
- Arteries from the ligated (CCI) side showed reduced responsiveness to electrical field stimulation compared to the contralateral side.
- Arteries from the ligated side exhibited increased sensitivity to alpha 1-adrenoceptor stimulation.
Conclusions:
- Sympathetic dysfunction in the CCI model of neuropathic pain is characterized by denervation-induced supersensitivity to catecholamines.
- This supersensitivity, rather than increased sympathetic nerve activity, appears to be the primary mechanism underlying sympathetic dysfunction in this model.
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