Sr. Brunnert, MORPHOLOGIC RESPONSE OF MYOCARDIUM TO FREEZE-THAW INJURY IN MOUSE STRAINS WITH DYSTROPHIC CARDIAC CALCIFICATION, Laboratory animal science, 47(1), 1997, pp. 11-18
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 dia
phragm in DBA/2, C3H/He, and C57BL/6 (control) mice. Two mice from eac
h mouse strain were euthanized 6, 12, 24, and 36 h after the initial f
reeze-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 diaphragmati
c 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 injur
y. Ultrastructurally the mineralized deposits first accumulated in mit
ochondria as early as 24 h after injury, with subsequent complete mine
ralization of the mitochondria and surrounding sarcoplasm by 48 h. The
se results suggest that the pathogenesis of dystrophic cardiac calcifi
cation in DBA/2 and C3H/He mice may be related to disturbed myocyte ca
lcium metabolism, leading to mitochondrial calcium overload and myocar
dial calcification.