Oguchi E, Okazaki M, Hobara R, Toyoshima Y, Sakamoto K
Nihon Yakurigaku Zasshi. 1978 Nov;74(8):991-1004.
We observed under light and electron microscopes morphological changes in the brains of rats in a thiamine deficient state as induced by an oxythiamine, pyrithiamine and thiamine deficient diet (OT, PT and TDD). We simultaneously determined thiamine levels in the whole brain of rats. The rats were separated into six groups-normal control, OT or PT treated rats (OT or PT group), OT or PT treated rats fed a TDD (OTD or PTD group), rats fed a TDD (TDD group)-. Microscopically, there were symmetrically distributed lesions containing spongy reticulation mainly in the vestibular nucleus. Electron microscopically, we found more advanced lesions in the OTD and PTD groups than in the TDD group. These ultrastructural changes were seen in the vicinity of capillaries and such consisted of abnormal endothelial cells and pericytes, excrescence of microglias, swelling or vacuolation of astrocytes, nerve cells containing distorted organelle and myelin degeneration, besides extracellular edema. The thiamine level in the TDD group decreased to 56% that of control. No effect of OT on the thiamine level was observed either in case of ingestion of a regular diet or when TDD was given. On the other hand, the thiamine level decreased to 43% in the PT group and to 17-23 in PTD. These results suggest that encephalopathy caused by the OT or PT-induced thiamine deficiency has the same selective vulnerable site as does the TDD-induced deficiency, however cellular sensitivity may differ slightly with the various ultrastructural changes.
我们在光学显微镜和电子显微镜下观察了由氧代硫胺、吡硫胺和硫胺缺乏饮食（OT、PT和TDD）诱导的硫胺缺乏状态下大鼠大脑的形态变化。我们同时测定了大鼠全脑的硫胺水平。大鼠被分为六组——正常对照组、接受OT或PT处理的大鼠（OT或PT组）、接受OT或PT处理并喂食TDD的大鼠（OTD或PTD组）、喂食TDD的大鼠（TDD组）。在显微镜下，主要在前庭核中存在含有海绵状网状结构的对称分布病变。在电子显微镜下，我们发现OTD组和PTD组的病变比TDD组更严重。这些超微结构变化见于毛细血管附近，包括异常的内皮细胞和周细胞、小胶质细胞增生、星形胶质细胞肿胀或空泡化、含有变形细胞器的神经细胞和髓鞘变性，此外还有细胞外水肿。TDD组的硫胺水平降至对照组的56%。无论喂食常规饮食还是给予TDD，均未观察到OT对硫胺水平有影响。另一方面，PT组的硫胺水平降至43%，PTD组降至17 - 23%。这些结果表明，由OT或PT诱导的硫胺缺乏引起的脑病与TDD诱导的缺乏具有相同的选择性易损部位，然而细胞敏感性可能因各种超微结构变化而略有不同。
