Histochemical Study on the Atrophy of the Quadriceps Femoris Muscle Caused by Knee Joint Injuries of Rats

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Title ( eng )
Histochemical Study on the Atrophy of the Quadriceps Femoris Muscle Caused by Knee Joint Injuries of Rats
Creator
Okada Yuji
Source Title
Hiroshima Journal of Medical Sciences
Volume 38
Issue 1
Start Page 13
End Page 21
Journal Identifire
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
Abstract
Atrophy developing in the quadriceps femoris muscle following knee injury is one of the serious problems not only in the field of orthopedics but also of rehabilitation. However the pathogenesis of this atrophy has not yet been elucidated. The author therefore produced a complex ligament injury model using the knee joints of rats in order to study the pathogenesis of this atrophy. After severing the anterior cruciate ligament, the medial collateral ligament and tibial insertion of the medial meniscus of rats, these animals were sacrificed at 4, 8 and 12 weeks. After removing the vastus lateralis muscle, vastus medialis muscle, and rectus femoris muscle, specimens of these muscles were stained for ATPase. The transection area of the muscle fibers was measured and the fiber type composition was determined. At 4 weeks the vastus medialis muscle and at 12 weeks the vastus lateralis muscle showed marked atrophy. The rectus femoris muscle exhibited the least atrophy throughout the entire observation period. In examining the atrophy of the quadriceps femoris muscle by muscle fiber type, the degree of atrophy was found to differ among the venters and even the same venter showed a different reaction depending on the elapsed time after sustaining the injury. Neither changes in the fiber type composition not neurogenic findings could be observed.
Keywords
Muscle atrophy
Knee injury
Histochemistry
ATPase
NDC
Medical sciences [ 490 ]
Language
eng
Resource Type departmental bulletin paper
Publisher
Hiroshima University Medical Press
Date of Issued 1989-03
Publish Type Version of Record
Access Rights open access
Source Identifier
[ISSN] 0018-2052
[NCID] AA00664312
[PMID] 2526800