RESUMO
The hexaferrite Ba1-x Sr x Fe12O19 compounds with x = 0, 0.5 and 1 were synthesized by the autocombustion method. X-ray diffraction (XRD), Raman spectroscopy and transmission electron microscopy (TEM) were used for structural and morphological studies.
RESUMO
We observed under light and electron microscopes morphological changes in the rat sciatic nerve during the last stages of a thiamine deficient state as induced by pyrithiamine (PT: 50 microgram/100g X 11 days) and thiamine deficient diet (TDD), in which rats experienced severe tetanic convulsions. Experiments were undertaken with normal control, PT (PT treated rats) and PTD (PT treated rats fed a TDD) groups. Grossly, 4 out of 9 rats in the PTD group had severe tetanic convulsions on the 12th day and there were no neurologic signs in the PT group. Microscopically, many of the myelinated axons in the animals in the PT group showed shrinkage with myelin ovoids and folds, but in the PTD group, there was swelling as well as shrinkage. Despite the difference in general-symptoms between the PT and the PTD groups, axonal degeneration in the both groups, as determined electron microscopically was almost to the same degree and the convulsed rats in the PTD group showed the severest changes in the myelin sheath. These ultrastructural changes included swelling or vacuolation of Schwann cells, axonal degeneration with the appearance of a myelin like structure, collection of neuro-tubules or vacuoles, invasion of Schwann cell or/and myelin fragments into the periaxonal space, and active phagocytosis by the macrophages. These results suggest that PT directly affects the nervous system and that the dysfunction of the sciatic nerve following PT-induced thiamine deficiency originates from the central nervous system.