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实验性低钾性肌病

Experimental potassium depletion myopathy.

作者信息

Corbett A J, Pollock M

出版信息

J Neurol Sci. 1981 Feb;49(2):193-206. doi: 10.1016/0022-510x(81)90078-2.

Abstract

Myopathic morphological changes were observed in the calf muscles of rats maintained on a potassium-depleted diet for 30-50 days. Light-microscopic changes were more severe in the superficial gastrocnemius muscle fibres and included pallor, swelling and vacuolation, progressing to necrosis, mononuclear cell infiltration and phagocytosis. Mitochondrial disruption, transverse tubular dilatation, membranous body formation and vacuolation were seen on ultrastructural examination. Both vacuoles and subsarcolemmal membranous bodies were shown to be in continuity with the transverse tubular system. More advanced myopathic changes were those of sarcomere destruction and muscle fibre necrosis. Morphological changes resemble those of human potassium depletion myopathy. Ineffective energy metabolism and focal ischaemia due to impaired vasodilatation are proposed as mechanisms for the myopathy of potassium depletion.

摘要

在低钾饮食维持30 - 50天的大鼠小腿肌肉中观察到了肌病形态学变化。浅部腓肠肌纤维的光镜变化更为严重,包括苍白、肿胀和空泡化,进而发展为坏死、单核细胞浸润和吞噬作用。超微结构检查可见线粒体破坏、横管扩张、膜状体形成和空泡化。空泡和肌膜下膜状体均显示与横管系统相连。更严重的肌病变化是肌节破坏和肌纤维坏死。形态学变化类似于人类低钾性肌病。能量代谢无效和血管舒张受损导致的局部缺血被认为是低钾性肌病的发病机制。

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