Captopril suppresses interstitial fibrin deposition in coxsackievirus B3 myocarditis.
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.
Takada
H
H
Second Department of Internal Medicine, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Japan.
Kishimoto
C
C
Hiraoka
Y
Y
Kurokawa
M
M
Shiraki
K
K
Sasayama
S
S
D000818:Animals; D002216:Captopril / Q000494:pharmacology*; D002522:Chlorocebus aethiops; D003238:Connective Tissue / Q000473:pathology; D003384:Coxsackievirus Infections / Q000401:mortality; D029822:Enterovirus B, Human; D005110:Extracellular Space / Q000378:metabolism*; D005337:Fibrin / Q000037:antagonists & inhibitors* / Q000378:metabolism; D009205:Myocarditis / Q000378:metabolism* / Q000473:pathology / Q000821:virology*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009218:Myosins / Q000378:metabolism; D009929:Organ Size
D005337:Fibrin; D002216:Captopril; D009218:Myosins