实验性变态反应性脑脊髓炎模型病理及组化研究

Astudyonhistopathology,ultrastructureandmonoaminefluorescenthistochemistryintheexperi┐mentalalergicencephalomyelitismodelfromguineapigs

为了研究实验性变态反应性脑脊髓炎（ＥＡＥ）的病理、组化的变化，通过对豚鼠ＥＡＥ模型进行普通病理、电镜及单胺类介质荧光组化研究发现，动物发病前的组织虽在光镜下无明显病变，但电镜下可见髓鞘薄层环形结构松散、断裂或融合；薄髓鞘的轴索内可见线粒体肿胀和嵴消失，而厚髓鞘纤维轴索内的线粒体尚完好。病变以脊髓白质为主，脑的病变主要集中于脑室周围。病变以坏死为主，集中于小静脉周围，可见髓鞘脱失；炎细胞包绕小静脉呈袖套样改变。此外，ＥＡＥ神经组织单胺类介质荧光密度显著减少，这可能是引起ＥＡＥ动物肢体运动功能障碍的原因之一。

Thepathologicalchangesofexperimentalalergicencephalomyelitis(EAE)werestudiedintheguineapigswiththeaidofalightmicroscope(LM),anelectronmicroscope(EM)andfluorescenthistochemistry.NoevidentlesionswerefoundunderLMbeforetheclinicalonsetofEAE,butunderEMtherewasalotofloose,fusionalandfragmentalspiremesofmyelinsheath.Themitochondriaintheaxonsofthickmyelinsheathsappearedtobenormal,butthemitochondriainaxonsofthinmyelinsheathswereenlarged.Thebainlesionsweremainlylocatedinthewhitemat-ter,especialyaroundthecerebralventricle.Thedamagesinthespinalcordwereverysevere.Necrosiswasthemainpathologicchangeandusualyenclosedminorveins.Demyelinatingcouldbeseenandinflammatorycelsenclosingminorveinslikecufinginfiltration.Mostinflammatorycelswerelymphocytesandmacrophages.Otherwise,thefluorescentdensityofmonoaminesinEAEwassignificantlydecreased.Perhapsthisfindingmighthelpexplaintheimpairmentofthemovementoftheextremities.