急性实验性水肿脊髓神经节包膜、血管、胶质和神经成分的结构改变。光学和电子显微镜研究

E. Gasimov, A. A. Aliyarbekova
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引用次数: 0

摘要

由于在静脉注射内毒素(LPS)的影响下,脊髓神经节的包膜下、血管周围、神经元周围和神经元间隙的血管通透性增加,确定了与水肿液放置相对应的未染色区域。在脊髓神经节囊内层形成的“神经周围窗口”的大小取决于脊髓神经节血管的数量和周长(交换表面积)。伪单极神经元和胶质卫星细胞之间关系的破坏导致暗变性神经元的形成。在超微结构上证实,引起脊髓神经节内巨噬细胞焦亡的原因不是大肠杆菌本身,而是作为其壁的LPS。
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Structural changes of capsular, vascular, glial and neural elements of the spinal ganglia in acute experimental edema. Light and electron microscopic studies
As a result of an increase in vascular permeability under the influence of intravenously administered endotoxin (LPS) in subcapsular, perivascular, perineuronal and interneuronalspaces of the spinal ganglia were identified unstained areas corresponding to theplacement of edematous fluid. Dimensions of the "perineural windows" formed in the inner layerspinal ganglion capsule depends on the number and perimeter (exchange surface area)vessels of the spinal ganglia. Disruption of the relationship between pseudo-unipolar neuronsand glial satellite cells leads to the formation of dark degenerative neurons.It was ultrastructurally proved that the cause of pyroptosis death of macrophages located insideIn the spinal ganglia, it is not the E. coli itself, but the LPS, which is part of its wall.
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