Myocardial lesions and the alteration of atrial granularity in dystrophic mice.

T Nomura, K Mizukawa, N Otsuka
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引用次数: 5

Abstract

Atria from dystrophic and non-dystrophic mice were examined by light and electron microscopy. Particular attention was paid to the granularity of the specific atrial granules and the development of the Golgi apparatus. At the light microscopic level, both a decrease in number and degenerative changes were recognized in the atrial cardiocytes, which were intercalated by increased connective and adipose tissues. At the electron microscopic level, the dystrophic atrial cardiocytes showed a variety of degenerative changes and a decreased number of granules; the impaired development of the Golgi apparatuses were noticed. A quantitative analysis revealed that the number of the granules per unit area in dystrophic cardiocytes was significantly smaller in both the right and left atria, and that the relative area occupied by the Golgi fields of the dystrophic was significantly smaller in the right atrium than in non-dystrophic controls. These findings indicate that the synthesis of atrial natriuretic polypeptide (ANP) is inhibited in dystrophic mice. It is suggested that the water and electrolyte imbalance known in dystrophic cases can be accounted for by the impaired secretion of ANP in the heart.

营养不良小鼠心肌损伤与心房粒度的改变。
用光镜和电镜观察了营养不良小鼠和非营养不良小鼠的心房。特别注意的是特定心房颗粒的粒度和高尔基体的发展。在光镜下,心房心脏细胞数量减少和退行性改变,被增加的结缔组织和脂肪组织嵌入。电镜下,营养不良的心房细胞出现多种退行性改变,颗粒数量减少;人们注意到高尔基体发育受损。定量分析显示,右心房和左心房营养不良心肌细胞单位面积颗粒数明显少于右心房,右心房营养不良心肌细胞高尔基区所占相对面积明显小于非营养不良对照组。这些结果表明,营养不良小鼠心房钠素多肽(ANP)的合成受到抑制。提示营养不良病例中已知的水和电解质失衡可能是由于心脏中ANP分泌受损所致。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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