Bradykinin and prostaglandins are established mediators of exudative and 
inflammatory phases of healing. Their contribution to the fibrogenic component 
of healing in the heart is less certain. We therefore undertook the present 
study in rats with acute myocardial infarction (MI) following left coronary 
artery ligation. Treatment with a bradykinin B2 receptor antagonist (Hoe140, 0.5 
microgram/kg/min s.c.) or a cyclooxygenase inhibitor (indomethacin, 2 mg/kg 
p.o.), initiated 24 h after surgery, was examined for responses in MI topography 
(size and area), MI and nonMI tissue fibrosis (fibrillar collagen specific 
picrosirius red). Early (week 1) and late (week 4) phases of fibrogenesis postMI 
were examined. Compared to control, we found: (1) MI size at weeks 1 and 4 was 
comparable in untreated and treated rats: (2) infarct area, a measure of scar 
thickness, was reduced (P < 0.05) at week 4 by each intervention; and (3) 
densitometric collagen volume fraction did not reveal a reduction in collagen 
accumulation at the MI site, but this was evident remote to the MI (P < 0.05) at 
week 4 for each agent. Thus, pharmacological interference with 
bradykinin-receptor binding or prostaglandin synthesis following MI is 
associated with reduced fibrillar collagen formation. Though the mechanism 
responsible for observed alteration in fibrogenesis is uncertain, 
anti-inflammatory and anti-proliferative properties of these agents may be 
responsible.