Saito K, Fukunaga H, Matsuoka T, Birou S, Kashima T, Tanaka H
Heart Vessels. 1985 Aug;1(3):129-32. doi: 10.1007/BF02066407.
In order to clarify the mechanism of myocardial changes in KK mice, cultured heart cells from both normal and spontaneously diabetic KK mice were studied by electron microscopy, photoelectric recording, and 45Ca activity. Compared with cultured heart cells from normal mice, those from KK mice showed a decrease in beating frequency and ceased beating more rapidly. The rhythm of the beating cells from KK mice became irregular, while that of the heart cells from normal mice was not changed significantly over a period of 10 days. Electron micrographs of cultured heart cells from KK mice showed an increased number of mitochondria, an intricate arrangement of myofibrils, poorly formed Z bands, and a lipidlike substance. The 45Ca activity of heart cells from KK mice, after incubation for 24 h in a medium containing 45Ca, was increased compared with heart cells from normal mice. Based on these findings, we conclude that ultrastructural alterations exist in cultured heart cells from KK mice and we suggest that an increase of intracellular Ca might play an important role in the pathogenesis.
为了阐明KK小鼠心肌变化的机制，通过电子显微镜、光电记录和45Ca活性研究了正常和自发性糖尿病KK小鼠的培养心肌细胞。与正常小鼠的培养心肌细胞相比，KK小鼠的心肌细胞搏动频率降低，且更快停止搏动。KK小鼠搏动细胞的节律变得不规则，而正常小鼠的心肌细胞节律在10天内没有明显变化。KK小鼠培养心肌细胞的电子显微照片显示线粒体数量增加、肌原纤维排列复杂、Z带形成不良以及出现类脂物质。在含有45Ca的培养基中孵育24小时后，KK小鼠心肌细胞的45Ca活性比正常小鼠心肌细胞增加。基于这些发现，我们得出结论，KK小鼠培养心肌细胞存在超微结构改变，并且我们认为细胞内Ca增加可能在发病机制中起重要作用。
