大鼠臂丛神经慢性卡压后不同时程神经组织的超微结构研究

目的 探讨大鼠臂丛神经慢性卡压后不同时程神经组织的超微结构变化。方法 建立大鼠慢性卡压模型，对卡压后不同时程神经组织的细胞成分进行超微结构的量化分析，有髓神经纤维数目计数，测定髓鞘厚度、脱髓鞘神经纤维、空化神经纤维，以及观察巨噬细胞、新生有髓神经纤维。结果 慢性卡压神经的超微结构较正常神经有明显变化，但又与急性神经损伤有所不同：(1)有髓神经纤维数目在早期无明显减少，在中期明显减少，在后期虽然总数仍减少，但与中期相比却呈上升趋势，这与后期出现的新生有髓神经纤维有关。(2)髓鞘厚度一直呈下降趋势，并与卡压时程呈正相关。(3)巨噬细胞活性在卡压12周时明显增强，内含大量退变髓鞘及坏死神经轴突。(4)在卡压后16周组出现较多新生有髓神经纤维，但髓鞘结构发育不完善，髓鞘厚度较薄。结论 脱髓鞘改变即髓鞘厚度的变化是卡压神经组织的早期变化，神经轴突的变化(空化神经纤维)是卡压神经组织的晚期变化。神经的慢性卡压过程是神经纤维变性、坏死和神经纤维再生的两种相反方向的不平衡的动态变化过程，并以损伤占主导地位。

The ultrastructure study of nerve tissues at intervals after chronic compression injury of brachial plexus at rats

Objective To study ultrastructure changes of nerve tissues at intervals after chronic compressioninjury of the rat brachial plexus nerve. Methode The chronic compression model of the rat brachial plexus nerve wasset up. The cell type in the nerve tissue was quantitatively evaluated by ultrastructure study at intervals after nervecompression: that is, the number of myelinated nerve fibers, the thickness of myelin sheath, the number ofdemyelinated nerve fibers, the number of cavitated nerve fibers, the changes of macrophage and the regeneratedmyelinated nerve fibers. Results Compared with the normal nerve, the ultrastructure of chronic compression nerve waschanged obviously, but it differed from that of the acute nerve in injury. (1) The number of myelinated nerve fiber was notObviously decreased at the early stage, and significantly decreased at the middle stage. Although the number decreasedat the later stage, it turned to increase compared with that at the middle stage. This phenomenon was due to theregenerated myelinated nerve fiber at the later stage; (2) The thickness of myelin sheath was inclined to decrease, witha ppsitive correlation with the compression time. (3) The activity of macrophage was increased obviously on 12 weeks.There were lots of degenerated myelin sheath and necrotic neuraxon in their bodies; (4) In the 16 weeki group, therewas lots of regenerated myelinated nerve fiber, but the myelin sheaths were not yet functionally developed intact with athin thickness of myelin sheaths. Conclusion It is demonstrated that the demyelinated process is that of the eary stageof chronic compression injury, and the neuraxon degeneration process is that of the late stage. It also unravels thatdegeneration, necrosis and regeneration of myelinated nerve fibers exist simultaneously during chronic compressionprocess, but they cann' t reach homeostasis, and the injury procedure is always dominant.