首页> 外文期刊>Laboratory Animal Science >MORPHOLOGIC RESPONSE OF MYOCARDIUM TO FREEZE-THAW INJURY IN MOUSE STRAINS WITH DYSTROPHIC CARDIAC CALCIFICATION
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MORPHOLOGIC RESPONSE OF MYOCARDIUM TO FREEZE-THAW INJURY IN MOUSE STRAINS WITH DYSTROPHIC CARDIAC CALCIFICATION

机译:心肌营养不良症对小鼠冻融损伤的形态学反应

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摘要

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.
机译:为了研究小鼠营养不良性心脏钙化的发病机制,我们研究了冻融损伤通过DBA / 2,C3H / He和C57BL / 6(表皮)腹部的冷冻融化损伤引起的心肌和骨骼肌(膜片)坏死。老鼠。在最初的冻融损伤后的6、12、24和36小时,对每只小鼠品系的两只小鼠实施安乐死。在损伤后第2、4、7、14和28天对来自每个品系的6只小鼠实施安乐死。通过光镜和电子显微镜技术研究心脏和隔膜。响应损伤的心肌和diaphragm肌矿化仅发生在DBA / 2和C3H / He小鼠中,并且早在初始心肌细胞损伤后2天就出现。超微结构化的矿化沉积物最早在受伤后24小时就开始积累在线粒体中,随后在48 h内线粒体和周围的肌浆完全矿化。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,从而导致线粒体钙超载和心肌钙化。

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