Variation in Serum Creatine Phosphokinase Activity as Indicated in Two-Phase EMC-D Virus-Induced Myocarditis.

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  • MIZUTANI Masato
    Department of Molecular Immunology, Graduate School of Agriculture and Life Sciences, University of Tokyo
  • HIRASAWA Kensuke
    Department of Biomedical Science, Graduate School of Agriculture and Life Sciences, University of Tokyo
  • TAKEDA Makio
    Department of Biomedical Science, Graduate School of Agriculture and Life Sciences, University of Tokyo
  • DOI Kunio
    Department of Veterinary Pathology, Graduate School of Agriculture and Life Sciences, University of Tokyo
  • YUKAWA Masayoshi
    Department of Biomedical Science, Faculty of Agriculture and Veterinary Medicine, University of Nihon
  • MATSUMOTO Yasunobu
    Department of Molecular Immunology, Graduate School of Agriculture and Life Sciences, University of Tokyo
  • MATSUMOTO Yoshitsugu
    Department of Molecular Immunology, Graduate School of Agriculture and Life Sciences, University of Tokyo
  • ONODERA Takashi
    Department of Molecular Immunology, Graduate School of Agriculture and Life Sciences, University of Tokyo

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タイトル別名
  • Variation in Serum Creatine Phosphokina

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説明

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.<br>

収録刊行物

  • Experimental Animals

    Experimental Animals 45 (4), 333-338, 1996

    公益社団法人 日本実験動物学会

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