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[肌肉病理过程发展中收缩装置的状态。III. 泽克尔氏坏死中收缩装置结构变化的性质及顺序]

[State of the contractile apparatus during the development of a pathological process in the muscles. III. The nature and sequence of the structural changes in the contractile apparatus in Zenker's necrosis].

作者信息

Borovikov Iu S, Kirillina V P, Chernogriadskaia N A

出版信息

Tsitologiia. 1979 Aug;21(8):900-7.

PMID:315121
Abstract

Using polarized ultraviolet (UV) fluorescence microscopy, it was shown that the local damage of muscle fibres causes in their morphologically unchanged parts the alternation of regions, being in different functional states referred to as "pseudocontraction" and "superrelaxation". The pattern of UV fluorescence anisotropy suggests that conformation of contractile proteins by "pseudocontraction" is similar to that at contraction, though changes in sarcomere length do not occur. The "superrelaxation" is characterized by a desorganization of myofilaments. During the spreading of Zenker's necrosis, the "pseudocontraction" is seen transferred first into "superrelaxation", and then into irreversible contracture and rigor. "The boundary of Zenker's necrosis" overlaps with the boundary of the self-propagating irreversible contracture. There is no proper boundary of Zenker's necrosis, because the destructive changes are observed over all the muscle fibre. Contraction nodules arise in the regions of "superrelaxation" and follow the changes of the contractile system, peculiar of contracture. The study of the influence of medium ionic composition on the development of Zenker's necrosis suggests that the arising and spreading of destruction are inseparably associated with the irreverrsible changes of intracellular membrane structures, and with the possibility of propogation of the damage signal by these structures along muscle fibres.

摘要

利用偏振紫外(UV)荧光显微镜观察发现,肌纤维的局部损伤会使其形态未改变的部分出现区域交替,这些区域处于不同的功能状态,分别称为“假收缩”和“超松弛”。紫外荧光各向异性模式表明,“假收缩”时收缩蛋白的构象与收缩时相似,尽管肌节长度没有变化。“超松弛”的特征是肌丝紊乱。在泽克尔氏坏死扩散过程中,首先可见“假收缩”转变为“超松弛”,然后转变为不可逆挛缩和尸僵。“泽克尔氏坏死边界”与自传播不可逆挛缩边界重叠。泽克尔氏坏死没有确切边界,因为在整个肌纤维上都观察到了破坏变化。收缩结节出现在“超松弛”区域,并随着挛缩特有的收缩系统变化而变化。对介质离子组成对泽克尔氏坏死发展影响的研究表明,破坏的产生和扩散与细胞内膜结构的不可逆变化以及这些结构沿肌纤维传播损伤信号的可能性密切相关。

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