Olbrich H G, Herrmann G, Vandeplassche G, Michaelis H, Schneider M, Krause E, Kober G
Abteilung für Kardiologie, Universität Frankfurt, Federal Republic of Germany.
J Clin Pathol. 1990 Aug;43(8):650-3. doi: 10.1136/jcp.43.8.650.
Myocardial calcium overload was observed in a patient with giant cell myocarditis. The myocardial calcium content estimated by atomic absorption spectrophotometry amounted to 120 mEq/kg dry weight, and the von Kossa stain disclosed multiple foci with patchy calcifications of myocardial fibres. Cytochemical examination of the ultrastructural calcium localisation using the phosphate-pyroantimonate method showed considerable variation in the subcellular calcium distribution. In normal myocytes calcium precipitates were confined to the inner leaflet of the sarcolemma, T-tubules, intercalated disks, and sporadically to mitochondria. In contrast, extensive calcification of mitochondria and loss of sarcolemmal calcium was evident in necrotic myocytes. A number of grossly normal myocytes also showed an increase of calcium precipitates in slightly swollen mitochondria. These findings suggest that myocardial calcium overload in this case started in viable myocytes and was not merely a secondary phenomenon occurring after cell death.
在一名巨细胞心肌炎患者中观察到心肌钙超载。通过原子吸收分光光度法估计的心肌钙含量达到120 mEq/kg干重,并且冯·科萨染色显示心肌纤维有多处散在钙化灶。使用焦锑酸盐磷酸盐法对超微结构钙定位进行细胞化学检查显示,亚细胞钙分布存在显著差异。在正常心肌细胞中,钙沉淀局限于肌膜的内小叶、T小管、闰盘,偶尔也见于线粒体。相比之下,坏死心肌细胞中线粒体广泛钙化且肌膜钙丢失明显。一些大体正常的心肌细胞在轻度肿胀的线粒体中也显示钙沉淀增加。这些发现表明,该病例中的心肌钙超载始于存活的心肌细胞,而不仅仅是细胞死亡后发生的继发现象。