AN EXPERIMENTAL STUDY ON COMPARTMENT SYNDROME OF INTRANERVE ROOT

结果：在采集和应用NP或肌肉的过程中，或在数据采集期间，全身动脉压无明显变化。血流量：NP组的血流量在3~4h后较初始值减少10~20%。与观察期结束时血流与基线无差异的对照组(P&lt；0.01)相比，这一下降具有统计学意义。尿内压：NP组初始EFP为2.6×1.2 cm H2O，对照组为2.1×0.6。用药3小时后，NP组EFP为7.5×4.6，对照组为2.0×0.8。组织学：在NP动物的神经根和许多相关的DRG中，水肿是主要的病理表现，在NP处理的神经根和DRG中偶尔可以观察到轴突和髓鞘病理。讨论：将NP应用于神经根增加了EFP，减少了DRG的血流量。换句话说，这种情况可以被称为由NP应用于神经根而导致的DRG的“间隔室综合征”。肌肉应用没有效果，这表明与应用NP相关的化学物质是导致这些病理生理变化的原因，实验过程本身并不起作用。我们没有确定这些急性变化是否会进展到包括轴突沃勒变性或神经元死亡。然而，持续的血流减少和/或炎症诱导的神经细胞激活可能会导致进一步的功能障碍和疼痛，正如已知的神经病理性疼痛的周围神经病模型中所发生的那样。因此，DRG中的这些急性观察可能是腰椎间盘突出症腰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.