1998 Fiscal Year Final Research Report Summary
AN EXPERIMENTAL STUDY ON COMPARTMENT SYNDROME OF INTRANERVE ROOT
Project/Area Number |
09671508
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Orthopaedic surgery
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Research Institution | FUKUSHIMA MEDICAL COLLEGE |
Principal Investigator |
KONNO Shinichi FUKUSHIMA MEDICAL COLLEGE,DEPT.OF ORTHOP.SURG.ASSISTANT PROFESSOR, 医学部・整形外科, 講師 (70254018)
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Co-Investigator(Kenkyū-buntansha) |
YABUKI Shoji FUKUSHIMA MEDICAL COLLEGE,DEPT.OF ORTHOP.SURG.ASSISTANT PROFESSOR, 医学部・整形外科, 助手 (00260779)
KIKUCHI Shinichi FUKUSHIMA MEDICAL COLLEGE,DEPT.OF ORTHOP.SURG.PROFESSOR, 医学部・整形外科, 教授 (80045773)
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Project Period (FY) |
1997 – 1998
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Keywords | COMPARTMENT SYNDROME / NERVE ROOT / NUCLEUS PROPOSUS / EDEMA |
Research Abstract |
Results : There was no significant change in systemic arterial blood pressure during the harvesting and application of NP or muscle, or during the period of data collection. Blood Flow : Blood flow in the NP group was reduced by 10-20% from the initial value after 3-4 hours. This reduction was statistically significant compared with control group (p<0.Ol) whose blood flow was not different from baseline at the end of the observational period. Endoneurial Fluid pressure : EFP was initially 2.6*1.2 cmH2O in the NP group, and 2.1*0.6 in control group. Three hours after application, EFP was 7.5*4.6 in the NP group (p<O.O5), and 2.0*0.8 in the control group (p>0.05). Histology : Edema was the principal pathological findings seen consistently in the nerve roots from NP animals and in many of the associated DRGs, Axonal and myelin pathology was occasionally observed in NP-treated roots and DRGs. Discussion : Application of NP to nerve root increased EFP and decreased blood flow in the DRG.In other words, this condition may be called a "compartment syndrome" in the DRG induced by application of NP to nerve root. Application of muscle was without effect, suggesting that chemical *ors associated with applied NP were responsible for these pathophysiologic changes, and that the experimental procedure, by itself, was not of consequence. We did not determine if these acute changes would progress to include Wallerian degeneration of axons or neuronal death. However, persistent reduction of blood flow and/or inflammation-induced activation of endoneurial cells might be expected to cause further functional deficit and pain, as is known to occur in peripheral neuropathy models of neuropathic pain. Thus, these acute observations in the DRG may be important initial factors in the pathogenesis of lumbar pain due to disc herniation.
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Research Products
(2 results)