In:
Journal of Orthopaedic Research, Wiley, Vol. 30, No. 10 ( 2012-10), p. 1660-1665
Kurzfassung:
It is known that free nerve endings are degenerated after application of shock waves. We therefore hypothesized that the application of shock waves to muscle induces dysfunction of neuromuscular transmission at neuromuscular junctions. We investigated changes in neuromuscular transmission in response to shock wave application. Sprague–Dawley rats were used in this study. Two thousand shock waves at an energy flux density of 0.18 mJ/mm 2 were applied to their right calf muscles. Neuromuscular junctions of gastrocnemius muscles were evaluated using rhodamine–α‐bungarotoxin on the day of treatment ( n = 5). Amplitude and latency of compound muscle action potentials were measured on the day of treatment and 1, 2, 4, 6, and 8 weeks after treatment ( n = 10, each group). Degenerated acetylcholine receptors existed in all treated muscles. Although the action potential amplitude on the treated side was significantly less than on the control side from the day of treatment (25.1 ± 7.8 vs. 34.5 ± 9.1, p = 0.012) to 6 weeks (27.9 ± 7.2 vs. 34.5 ± 7.2, p = 0.037), there was no significant difference at 8 weeks. There was no significant difference in transmission latency between the groups. The application of shock waves to muscle induced a transient dysfunction of nerve conduction at neuromuscular junctions. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:1660–1665, 2012
Materialart:
Online-Ressource
ISSN:
0736-0266
,
1554-527X
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2012
ZDB Id:
2050452-4