RESUMO
Collagen constitutes the majority of extracellular matrix in tissues such as bone, cartilage, and especially the skin. Over production and/or decreased degradation of collagen fibers could lead to an abnormal wound healing response resulting in hypertrophic scarring or keloid formation. Recently, angiotensin II has been shown to be present in several cutaneous cells and that it stimulates fibroblast proliferation, collagen synthesis, and suppresses matrix metalloproteinase activity. The following study examines the effect of topical captopril, an inhibitor of angiotensin II production, against hypertrophic scar formation in New Zealand white rabbits.Two dermal wounds were made over the ventral surface of the ears of each rabbit (n = 6). In each animal, separate wounds were treated once per day with either topical 5% captopril or the vehicle alone (70% ethanol and 30% propylene glycol) for 7 consecutive days. Wounds were harvested at postoperative day 28, and the scar elevation index (SEI) as well as collagen organization was evaluated. SEI was reduced from 3.06 in the vehicle-treated group to 1.94 in the captopril treated wounds (P < 0.05). However, an increase in collagen organization was achieved by captopril, while an 8.50% decrease in collagen organization scale was derived by captopril compared to the vehicle. Results of this study show, for the first time, the efficacy of topical captopril as a new agent for the prevention of hypertrophic scar formation in an animal model. Thus, captopril might represent the first angiotensin converting enzyme inhibitor with a novel pharmacologic application in dermatology.