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Heart muscle performance after experimental viral myocarditis
The Journal of Clinical Investigation
|March 1, 1976
Summary
Experimental coxsackie virus B3 myocarditis in young hamsters can lead to lasting heart muscle dysfunction. Early viral infection in juvenile hamsters causes persistent decreases in myocardial contractility and compliance.
Area of Science:
- Cardiology
- Virology
- Pathology
Background:
- Idiopathic cardiomyopathy may have viral antecedents.
- Coxsackie virus B3 is a known cause of myocarditis.
Purpose of the Study:
- To investigate late structural and functional consequences of experimental coxsackie virus B3 myocarditis.
- To determine the impact of age at inoculation on the persistence of myocardial dysfunction.
Main Methods:
- Myocarditis was induced in 12- and 22-day-old hamsters using coxsackie virus B3.
- Isometric contractility (peak developed tension) and muscle mechanics were assessed at various time points post-inoculation.
- Glycerinated muscle preparations were used to evaluate contractile protein function.
Main Results:
- Inoculation at 12 days led to significant depression in peak developed tension (17-43%) at 18 and 90 days post-inoculation, with reduced muscle stretch requirement.
- Inoculation at 22 days resulted in a 15% depression in peak developed tension at 18 days, with 50% less tension in glycerinated muscles.
- Myocardial function recovered by 90 days in hamsters inoculated at 22 days, but persistent dysfunction was observed in those inoculated at 12 days.
- No differences from controls were noted at 180 days post-inoculation for either age group.
Conclusions:
- Acute coxsackie virus B3 myocarditis can cause persistent alterations in myocardial contractility and compliance.
- Age at the time of viral infection significantly influences the recovery and long-term sequelae of myocarditis.
- Younger hamsters (12 days) inoculated with coxsackie virus B3 exhibit prolonged myocardial dysfunction compared to older hamsters (22 days).