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DOI 10.1023/a:1022377001084

Медицинская библиотека · Inflammation · 1998

An experimental model of tennis elbow in rats: a study of the contribution of the nervous system.

Haker E, Theodorsson E, Lundeberg T

СтатьяПоддержка исследования: вне правительства СШАОтозванная публикацияПеревод в очереди
Источник пометил публикацию как отозванную.

Аннотация

The contribution of the sensory and autonomic nervous system to experimentally induced tennis elbow or lateral epicondylalgia was investigated by analyses of the release of neuropeptides from sensory (substance P, SP, neurokinin A, NKA, calcitonin gene-related peptide, CGRP) and sympathetic (neuropeptide Y, NPY) nerves. SP, CGRP, NKA, NPY-like immunoreactivity (-LI) was studied in rats cerebrospinal fluid (CSF), plasma and perfusates (PF) from the enthesis of the extensor carpi radialis brevis (ECRB) of the right elbow at 2, 6 and 24 h following 0.01 ml injection of either complete Freund adjuvans (FA) or 2% Carrageenan (CAR). The control group was injected with 0.01 ml saline. In general the changes of neuropeptide-LI in the CSF and plasma were similar for both treated groups compared with the controls, but they were more pronounced in the FA group than the CAR. SP-, NKA-, CGRP- and NPY-LI were significantly increased to a similar degree in the perfusates of the ECRBs of the treated groups with a greater increase in SP-LI in the FA than the CAR group compared with controls. When comparing the neuropeptide-LI in the CSF, plasma and PF between the 2 treated groups, there were thus few differences found. Generally a unilateral injection with either FA or CAR into the rat ECRB induced a similar alteration in the concentration of SP-, NKA-, CGRP- and NPY-LI in the CSF, plasma and PF at 2, 6 and 24 h following injection. However, the most pronounced changes in neuropeptide-LI occurred locally in the elbow ECRBs PF in both treated groups.

Для цитирования: Haker E, Theodorsson E, Lundeberg T. An experimental model of tennis elbow in rats: a study of the contribution of the nervous system.. Inflammation. 1998. DOI: 10.1023/a:1022377001084.

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