AJP - Heart and Circulatory Physiology, Vol 272, Issue 1 211-H219, Copyright © 1997 by American Physiological Society
Captopril suppresses interstitial fibrin deposition in coxsackievirus B3 myocarditis
H. Takada, C. Kishimoto, Y. Hiraoka, M. Kurokawa, K. Shiraki and S. Sasayama
Second Department of Internal Medicine, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Japan.
The effects of captopril on murine coxsackievirus B3 (CB3) myocarditis were
investigated, with focus on interstitial fibrin deposition and changes in
the connective tissue matrix. Captopril was administered intraperitoneally
at a dose of 0.1 mg/g to CB3-infected mice daily on days 10-30 in
experiment I (inflammatory phase) and on days 30-60 in experiment II
(fibrotic phase). In experiment I, mouse survival was higher in the
captopril-treated group than in the untreated group. Histological
improvement, including prevention of extravasated fibrin deposition,
maintenance of connective tissue architecture, suppression of myocyte
hypertrophy, and prevention of myosin isoform shift from alpha to beta, was
observed in captopril-treated mice in experiment I, but not in experiment
II; in experiment II, captopril administration suppressed thickening of the
interstitial reticulin fibers. Captopril inhibited inflammatory fibrin
deposition, postmyocarditic myocyte hypertrophy, and ventricular remodeling
during the inflammatory phase, but not during the fibrotic phase, of CB3
myocarditis in mice.
