Controlled wound repair in guinea pigs, using antimicrobials that alter fibroplasia

The repair processes of incised wounds depend, in part, on fibroplasia induced by soluble mediators from monocytic macrophages. Two topical antimicrobials were evaluated, each of which effectively controlled wound sepsis and yet each had widely different effects on fibroplasia and wound strength. Paired-incision dermal wounds on the flanks of guinea pigs were treated with a substance containing reactive chlorine (Alcide) or with a compound that is a mixture of two surfactants. One side of each guinea pig was treated with one of the antimicrobials (treated wounds); the opposite side was treated with isotonic saline solution (control wounds). At 7, 10, and 16 days after surgery, tensiometric measurements of C31G (a surfactant)-treated wounds were 99%, 139%, and 195% of control wound values, respectively. Alcide-treated wounds were 76%, 58%, and 88% of control wounds, respectively. Wounds treated with chlorhexidine had reduced strength at 7 days (73%) and at 10 days (78%), but by 14 days, they were similar to control wounds (94%). The main difference between the wounds was the amount of collagen formation. Alcide-treated wounds incorporated less than 50% of the amount of 14C-proline than did the wounds treated with C31G. However, Alcide-treated wounds epithelialized as rapidly as did control wounds, and had minimal scar formation. Microscopic evaluations indicated greatly reduced inflammatory infiltrates in Alcide-treated wounds, indicating that reduced wound strength may be associated with lack of fibroblast-stimulating activity by monocytes.