Brunnert S R, Altman N H
Department of Pathology, University of Miami School of Medicine, FL.
Lab Anim Sci. 1990 Nov;40(6):616-9.
Dystrophic cardiac calcinosis (DCC) is a frequent finding in DBA/2, C3H and BALB/c mice and its etiology is not known. Previous studies have speculated that myocardial necrosis is involved in the pathogenesis of DCC. In this study, cardiac necrosis was induced in DBA/2, C3H and C57BL/6 mice by freeze-thaw injury through the abdominal diaphragm. Four weeks after freeze-thawing, the mice were sacrificed and the hearts and diaphragms were examined. In response to injury, cardiac mineralization was present only in DBA/2 and C3H mice. The myocardium of C57BL/6 mice (control strain) healed by fibrosis without mineralization, the normal response of the myocardium to injury. Calcified diaphragms also were present at the site of freeze-thaw injury in DBA/2 and C3H mice, which is supportive evidence that a systemic abnormality is involved in the pathogenesis of DCC. The conclusion from this study is that the pathogenesis of DCC in DBA/2 and C3H mice is multifactorial and involves both myocardial necrosis and an abnormal response to injury.
营养不良性心脏钙化(DCC)在DBA/2、C3H和BALB/c小鼠中很常见,其病因尚不清楚。先前的研究推测心肌坏死参与了DCC的发病机制。在本研究中,通过经腹横膈膜冻融损伤在DBA/2、C3H和C57BL/6小鼠中诱导心脏坏死。冻融后四周,处死小鼠并检查心脏和横膈膜。作为对损伤的反应,只有DBA/2和C3H小鼠出现心脏矿化。C57BL/6小鼠(对照品系)的心肌通过纤维化愈合而无矿化,这是心肌对损伤的正常反应。DBA/2和C3H小鼠的冻融损伤部位也出现钙化的横膈膜,这是支持全身异常参与DCC发病机制的证据。本研究的结论是,DBA/2和C3H小鼠中DCC的发病机制是多因素的,涉及心肌坏死和对损伤的异常反应。