传染性腹膜炎猫大脑皮层病理形态学研究

G. Kotsyumbas, M. Khalaniia
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摘要

本文报道了10只3个月~ 5.5岁的猫尸体的大脑皮层额部的组织学研究结果,这些猫在生活中被诊断为感染性腹膜炎(基于记忆、临床症状、形态和生化血液分析、超声诊断、竞争试验和快速诊断)。进行病理解剖研究;选择猫大脑皮层额叶区样品,将其固定在12%的中性福尔马林水溶液中,即卡诺瓦和96°乙醇的溶液中。制作组织切片,苏木精染色,伊红染色,硫氨酸染色。为了检测星形胶质细胞的荣耀,用高尔基-克拉佐方法用新鲜的水合氯醛-重铬酸盐福尔马林混合物固定大脑皮层的一部分,并在冷冻切片机上产生组织切片。对猫的大脑皮层进行组织学检查,观察到非炎症性的变化,其特征是血液循环障碍、水肿和神经胶质复合体和神经元的退行性过程。内皮细胞、毛细血管和小静脉基底膜结构组织的破坏应被视为微循环通道张力和通透性功能改变的重要指标,这有助于血管周围和细胞周围水肿的发展,从而导致胶质成分的退行性改变;神经元急性肿胀伴核内微腔形成;锥体细胞和星状细胞中亲色物质含量的急剧减少;星形细胞和生物嗜视性营养不良的发生;影子细胞的崛起。循环障碍引起营养运输系统的破坏,导致缺氧,酸性代谢产物的积累,形成了神经胶质细胞和神经元的循环障碍性营养不良的发病机制,即猫大脑皮层的神经营养性疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pathomorphology of the cerebral cortex of cats for infectious peritonitis
The article presents the results of histological studies of the frontal area of the cerebral cortexб taken from 10 corpses of cats aged from 3 months to 5.5 years, in which infectious peritonitis (based on anamnesis, clinical signs, morphological and biochemical blood analysis , ultrasound diagnostics, Rivalt test and express diagnosis) was diagnosed during their life. A pathoanatomical study was conducted; samples of the frontal area of the cerebral cortex of cats, which were fixed in a 12% aqueous solution of neutral formalin, a solution of Carnoua and 96° ethyl alcohol, were selected. The histocuts were made, which were stained with hematoxylin and eosin, thionine for Nisslem. In order to detect the astrocytic glory, a fraction of the cerebral cortex was fixed by the Golgi-Clatzo method with a fresh mixture of chloral hydrate-formalin-bichromate and produced histocuts on a freezing microtome. For histological examination of the cerebral cortex of cats, changes in the non-inflammatory character were observed, which were characterized by disorders of hemomycrocycle circulation, edema and degenerative processes of the neuroglial complex and neurons. Violations of the structural organization of endothelial cells, basal membranes of capillaries and venules should be considered as an important indicator of functional changes in tone, permeability of the microcirculatory channel, which contributed to the development of perivascular and pericellular edema, which in its turn led to regressive changes of glial elements; acute swelling of neurons with the formation of microcavities in nuclei; a sharp decrease in the content of the chromatophilic substance in pyramidal and stellate cells; the development of gidropic dystrophy in star cells and creatures; rise of shadow cells. Circulatory disorders caused the violation of the trophic transport systems, which caused hypoxia, accumulation of acidic metabolism products, and formed the basis for the pathogenesis of the development of dyscirculatory dystrophy of neuroglial cells and neurons, i.e. neurotrophic disorders of the cerebral cortex of cats for FIR.
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