| Co-Investigator(Kenkyū-buntansha) |
IDE Junji Kumamoto University school of medicine : Department of orthopaedic surgery, assi, 医学部, 助手 (10253725)
MORISASA Keizo Kumamoto University school of medicine : Department of orthopaedic surgery, Inst, 医学部・付属病院, 講師 (50174412)
片岡 泰文 熊本大学, 医学部, 助手 (40204416)
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| Research Abstract |
This study was undertaken to investigate the analysis of the nervous irritation caused by nerve stretching at an intensity level not severe enough to cause avulsion injury. During traction on 64 forelegs of 32 rats, we evaluated changes in the blood flow in the extrinsic and intrinsic microvascular systems of the brachial plexus. While laterally stretching the brachial plexus during 80-degree shoulder abduction, we measured the blood flow at the bifurcation of the brachial plexus and at the median nerve, using the hydrogen washout technique. During weak traction, the blood flow decreased markedly in the extrinsic system, causing an imbalance in the two systems. In the median nerve, however, no such imbalance occurred. Histologically, the axon and myelin in the brachial plexus and the median nerve showed no morphological change. However, in parts of the brachial plexus, we noted hypertrophic connective tissue or granulomatous inflammation in tissue surrounding the extrinsic system. The
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extrinsic system's apparent susceptibility to injury by acute traction may be a factor in the pathogenesis of the brachial plexus stretching injuries.
The conjugation of H R P with wheat germ agglutinin was used to identify the effect on retrograde axonal transeport of stretching the rat sciatic nerve ideirectly by 10% and 20% femoral lengthenning with a unilateral external fixator. To investigate the relationship between retrograde axonal transport and blood flow in the stretched nerve, nerve blood flow in the sciatic nerve was measered by a hydrogen washout technique. At 11% strain (20% femoral lengthening), the numbers of horseradish peroxidase-labelled motor neuron cells and nerve blood flow had decreased by 43% and 50%, respectively. Histological examination demonstrated ischaemic changes, but not mechanical damage. However at 6% strain (10% femoral lenghethening) there were no significant abnoralities. There findings suggest that the inhibition of retrograde axonal transeport can be induced by acute streching of the peripheral nerve and that circulatory disturbance is the main cause of the inhibition of retrograde axonal transeport at the low strain. Less
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