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Heat stress aggravates viral myocarditis in mice
T Kanda1, M Nakano, T Yokoyama
1Department of Laboratory Medicine, Gunma University School of Medicine, Showa-machi, Maebashi, Japan. kanda@sb.gunma-u.ac.jp
Life Sciences
|March 9, 1999
Summary
Hyperthermia applied after viral inoculation worsened viral myocarditis in mice, increasing mortality and myocardial damage. However, hyperthermia before infection did not show these negative effects.
Area of Science:
- Cardiovascular Research
- Virology
- Immunology
Background:
- Viral myocarditis is a serious condition with limited treatment options.
- The potential therapeutic effect of hyperthermia on viral infections is debated, with no in vivo data for viral myocarditis.
Purpose of the Study:
- To investigate if hyperthermia can attenuate the course or severity of viral myocarditis.
- To examine the pathological changes and mortality in a murine model of viral myocarditis under different hyperthermia timings.
Main Methods:
- C3H mice were infected with encephalomyocarditis virus.
- Hyperthermia (42.5°C for 30 min) was administered either 4 hours before (HB) or 4 hours after (HA) viral inoculation.
- Control groups (Cont) received no hyperthermia. Cardiac viral titers, body weight, heart weight, and pathological changes were assessed.
Main Results:
- The HA group exhibited significantly higher mortality and cardiac viral titers compared to HB and Cont groups.
- Myocardial necrosis, heart weight, and body weight/heart weight ratio were significantly elevated in the HA group.
- Heat shock protein 70 (HSP70) was strongly expressed in the myocardium of the HA group but not in HB or Cont groups.
Conclusions:
- Inducing hyperthermia after viral inoculation aggravates viral-induced myocardial necrosis and increases mortality in a murine model.
- Hyperthermia post-infection induces myocardial heat shock protein 70 expression.
- The timing of hyperthermia is critical; post-infection application is detrimental in this model.