Brunnert S R
Institute of Comparative Medicine, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.
Lab Anim Sci. 1997 Feb;47(1):11-8.
To investigate the pathogenesis of dystrophic cardiac calcification in mice, we studied myocardial and skeletal muscle (diaphragm) necrosis induced by freeze-thaw injury through the abdominal portion of the diaphragm in DBA/2, C3H/He, and C57BL/6 (control) mice. Two mice from each mouse strain were euthanized 6, 12, 24, and 36 h after the initial freeze-thaw injury; 6 mice from each strain were euthanized 2, 4, 7, 14, and 28 days after injury. The hearts and diaphragms were studied by light and electron microscopic techniques. Myocardial and diaphragmatic mineralization in response to injury occurred only in DBA/2 and C3H/He mice and was present as early as 2 days after initial myocyte injury. Ultrastructurally the mineralized deposits first accumulated in mitochondria as early as 24 h after injury, with subsequent complete mineralization of the mitochondria and surrounding sarcoplasm by 48 h. These results suggest that the pathogenesis of dystrophic cardiac calcification in DBA/2 and C3H/He mice may be related to disturbed myocyte calcium metabolism, leading to mitochondrial calcium overload and myocardial calcification.
为了研究小鼠营养不良性心脏钙化的发病机制，我们通过对DBA/2、C3H/He和C57BL/6（对照）小鼠的膈肌腹部进行冻融损伤，研究了心肌和骨骼肌（膈肌）坏死情况。在初次冻融损伤后6、12、24和36小时，对每个品系的2只小鼠实施安乐死；在损伤后2、4、7、14和28天，对每个品系的6只小鼠实施安乐死。通过光学和电子显微镜技术对心脏和膈肌进行研究。仅在DBA/2和C3H/He小鼠中出现了对损伤的心肌和膈肌矿化，并且最早在初始心肌细胞损伤后2天就出现了。在超微结构上，矿化沉积物最早在损伤后24小时在线粒体中积累，到48小时线粒体和周围肌浆完全矿化。这些结果表明，DBA/2和C3H/He小鼠营养不良性心脏钙化的发病机制可能与心肌细胞钙代谢紊乱有关，导致线粒体钙超载和心肌钙化。
