Objective    To study the correlation between desmin degradation and calcium overload in rats with myocardial contusion (MC).     Methods    One-hundred-and-ten SD rats were randomly divided into a trauma (T) group (n=50)

a t

rauma + diltiazem (D) group (n=50)

and a control (S) group (n=10). The MC models were established by chest impact with BIM-III Bio-impactor. The animals in the D group were given diltiazem hydrochloride (0.5 mg/kg) through intraperitoneal injection after trauma. The Ca

2+

concentration

protein expression of desmin

and mRNA expression of desmin in myocardial cells were measured by confocal laser scanning microscopy

immunohistochemistry and Western blotting

and RT-PCR

respectively

before and after (2

4

8

24

and 48 h) trauma.     Results    Compared with that in the S group

the Ca

2+

concentration in myocardial cells in the T group increased significantly 2 h after trauma (110.4±17.6 vs 74.0±9.3

P0.01)

reached the peak 4 h after trauma (141.1±17.8)

and then decreased gradually to the level before trauma 48 h after trauma (78.6±10.3). Compared with that in the S group

the protein expression of desmin in the T group decreased to the lowest level 8 h after trauma (0.11±0.11 vs 1.23±0.27

P0.01)

began to increase 24 h after trauma (1.06±0.33)

and was higher than the level before trauma 48 h after trauma (1.82±0.41). Irregular aggregation of desmin was found in the T group at 48 h after trauma. Compared with the T group

the D group had a significantly lower Ca

2+

concentration in 4 and 8 h after trauma (84.6±9.7，89.3±11.8). The protein expression of desmin showed no significant difference between the T group and D group in 2 and 4 h after trauma

but was higher in the D group than in the T group 8 h after trauma (0.55±0.18 vs 0.11±0.11

P0.05). Compared with that of the S group (0.62±0.23)

the mRNA expression of desmin in the D group and T group increased after trauma and reached the peak at 24 h after trauma (1.24±0.30 and 1.63±0.31). The mRNA expression of desmin in the T group was higher than that in the D group in 24 and 48 h after trauma (1.63±0.31 vs 1.24±0.30

P0.05; 1.04±0.22 vs 0.78±0.21

P0.05).     Conclusion    Desmin disruption is directly caused by mechanica

l trauma in the early stage of MC

and the increase of intracellular Ca

2+

concentration after trauma can promote desmin degradation. The use of calcium channel blocker diltiazem hydrochloride can decrease intracellular Ca

2+

concentration and thus reduce desmin degradation after trauma.