AN EXPERIMENTAL STUDY ON COMPARTMENT SYNDROME OF INTRANERVE ROOT

结果如下：在采集和应用NP或肌肉期间，或在数据收集期间，全身动脉血压没有显著变化。血流：NP组的血流在3-4小时后比初始值减少10-20%。与对照组相比，该降低具有统计学显著性（p<0.01），在观察期结束时，对照组的血流量与基线无差异。应用后3小时，NP组的EFP为7.5*4.6（p<0.05），对照组为2.0*0.8组织学：水肿是在NP动物的神经根和许多相关DRG中一致观察到的主要病理学发现，在NP处理的根和DRG中偶尔观察到轴突和髓鞘病理学。神经根内应用NP可使DRG的EFP增加，血流量减少，即神经根内应用NP引起的DRG“筋膜室综合征”。肌肉应用没有影响，表明与应用NP相关的化学物质是这些病理生理变化的原因，实验过程本身并不重要。我们没有确定这些急性变化是否会发展到包括轴突的沃勒变性或神经元死亡。然而，血流的持续减少和/或炎症诱导的神经内膜细胞活化可能会导致进一步的功能缺陷和疼痛，如已知发生在神经性疼痛的周围神经病变模型中。因此，DRG中的这些急性观察结果可能是椎间盘突出引起腰椎疼痛发病机制的重要初始因素。

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.