1996 年 45 巻 4 号 p. 333-338
In this study, myocardial damage in the D-variant of encephalomyocarditis (EMC-D) virus-induced myocarditis has been investigated consecutively by measuring serum creatine phosphokinase (CPK) activity. CPK activity in 8 week-old male BALB/cAJcl mice inoculated with EMC-D virus increased to a peak at 4 or 5 days postinoculation (DPI) and then gradually 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 (early and late phase) myocardial damage in EMC virus infection were considered. In the late phase, an increase in cellular infiltration in the myocardium and a decrease in viral titer in the heart were observed. It was therefore suspected that the increase in CPK in the late phase may be caused by cellular infiltration, but not by viral replication. In our results, we suggested that a serial measurement of serum CPK activity might be a useful method for throwing more light on the myocardial damage caused by the autoimmune response. We also used a pathological (TUNEL) method to detect apoptotic cells and some apoptotic myocytes in the myocardium in late phase EMC virus-induced myocarditis.