The healing phase of acute myocardial infarction (AMI) is initiated by proteolysis of necrotic myocardium, followed by infiltration of fibroblasts and deposition of collagen. To assess whether ibuprofen, a potent antiinflammatory agent, preserves existing collagen and enhances deposition of new collagen during Infarct healing, biochemical and morphologic studies were made of experimentally induced myocardial infarcts in untreated rats and in rats treated with ibuprofen. All treated rats received 12.5 mg/kg of ibuprofen at 1, 6 and 18 hours after AML Group 1 rats underwent measurement of myocardial hydroxyproline (HP) content at 24 hours after AMI. Group 2 rats received ibuprofen, 12.5 mg/kg, twice a day for 2 additional days, with measurement of myocardial HP at 3 days (group 2a) or 21 days (group 2b) after AMI. Group 3 rats received ibuprofen, 12.5 mg/kg, twice a day for 6 additional days with measurement of HP content, or infarct size and degree of thinning at 21 days after AMI. Compared with untreated rats, ibuprofen-treated rats had significantly greater amounts of HP in the infarct at 24 hours (group 1, 8.9 ± 2.2 nmol/mg dry weight vs untreated, 7.1 ± 2.8 nmol/mg dry weight, p < 0.04) and at 21 days (group 2b, 112 ± 37 nmol/mg dry weight vs untreated, 91 ± 39 nmol/mg dry weight, p < 0.05, and group 3, 125 ± 51 nmol/mg dry weight vs untreated, 91 ± 39 nmol/mg dry weight, p <0.003). Substantial scar thinning was noted in all rats; no difference in scar thinning was noted between treated and untreated rats at 21 days after AMI. Morphologic examination of the infarct scar by light and electron microscopy revealed no qualitative differences between untreated and ibuprofen-treated rats. Thus, ibuprofen retards collagen proteolysis immediately after AMI and promotes collagen deposition without a deleterious effect on subsequent scar formation in rats with experimental AMI.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine