M. Mizutani et al., VARIATION IN SERUM CREATINE-PHOSPHOKINASE ACTIVITY AS INDICATED IN 2-PHASE EMC-D VIRUS-INDUCED MYOCARDITIS, Experimental animals, 45(4), 1996, pp. 333-338
In this study, myocardial damage in the D-variant of encephalomyocardi
tis (EMCD) virus-induced myocarditis has been investigated consecutive
ly by measuring serum creatine phosphokinase (CPK) activity. CPK activ
ity in 8 week-old male BALB/cAJcI mice inoculated with EMC-D virus inc
reased to a peak at 4 or 5 days postinoculation (DPI) and then gradual
ly decreased. The CPK activity rose again after 7 DPI until it reached
a second peak. In view of the kinetics of CPK activity, two-phase (ea
rly and late phase) myocardial damage in EMC virus infection were cons
idered. In the late phase, an increase in cellular infiltration in the
myocardium and a decrease in viral titer in the heart were observed I
t was therefore suspected that the increase in CPK in the late phase m
ay be caused by cellular infiltration, but not by viral replication. I
n our results, we suggested that a serial measurement of serum CPK act
ivity might be a useful method for throwing more light on the myocardi
al damage caused by the autoimmune response. We also used a pathologic
al (TUNEL) method to detect apoptotic cells and some apoptotic myocyte
s in the myocardium in late phase EMC virus-induced myocarditis.