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Mechanical analysis of the effects of bacteria and aprotinin on skin wound healing in adult guinea pigs

Inhibition of wound healing by bacteria may result in part from the conversion of plasminogen to plasmin. This conversion results in dissolution of the fibrin seal in a wound or between skin graft and bed. Aprotinin blocks conversion to plasmin, preserving the fibrin clot. The current study was undertaken to determine the effects of high concentrations of bacteria on wound healing and how these effects are mitigated by aprotinin. Dorsal full‐thickness skin incisions were made in 40 anesthetized guinea pigs and closed with nylon sutures. Animals were divided into four groups: (1) control wounds, (2) infected wounds, (3) wounds treated with aprotinin, and (4) infected wounds plus aprotinin (single dose). Animals were killed 3 and 4 weeks after the operation. Skin strips containing segments of the healing wounds were pulled apart by a tensiometer until rupture. Stress‐strain curves were generated, and wound strength and toughness were determined. All wounds, including those inoculated with bacteria, appeared healed. The 3‐week infected group healed with the least strength and toughness (p < 0.001). A single dose of aprotinin administered with the bacterial inoculum reversed this inhibition. In the 4‐week groups, the strongest and toughest wounds resulted from bacterial inoculation alone. Aprotinin alone augmented wound healing when compared with controls. These data suggest that wound healing in both clean and infected wounds is augmented when the plasminogen‐plasmin pathway is inhibited.