Levine S, Sowinski R
Am J Pathol. 1982 May;107(2):135-41.
Bipiperidyl mustard and a neurotoxic triamine are known to cause edematous and/or necrotizing lesions in particular areas of hypothalamus and dorsal medulla but not in spinal cord. Experimental allergic encephalomyelitis (EAR) causes widespread inflammatory lesions that are especially numerous in spinal cord. When the chemical toxicants were administered to rats during the acute phase of EAE, mortality was increased. This was due to a specific interaction between EAE and chemical toxicants leading to the development of necrotizing vasculitis and parenchymal necrosis near EAE lesions in spinal cord or brain. The interaction decreased as the EAE lesions healed. Another neurotoxic chemical, dipiperidinoethane, did not produce this phenomenon. These effects of EAE are probably related to damage to the vessel walls and the blood-brain barrier. The present work may increase the versatility of EAE as a model for multiple sclerosis if the EAE lesions can be enlarged progressively by repeated exposures to the toxicant.
已知联哌啶基芥子气和一种神经毒性三胺会在下丘脑和延髓的特定区域引起水肿性和/或坏死性病变，但不会在脊髓中引起此类病变。实验性变应性脑脊髓炎（EAE）会导致广泛的炎性病变，这些病变在脊髓中尤其多见。当在EAE急性期给大鼠施用化学毒物时，死亡率会增加。这是由于EAE与化学毒物之间的特定相互作用导致脊髓或脑内EAE病变附近出现坏死性血管炎和实质坏死。随着EAE病变愈合，这种相互作用会减弱。另一种神经毒性化学物质二哌啶基乙烷不会产生这种现象。EAE的这些效应可能与血管壁和血脑屏障受损有关。如果通过反复接触毒物可以使EAE病变逐渐扩大，那么目前的研究工作可能会增加EAE作为多发性硬化症模型的通用性。
