c-31g and Staphylococcal-Infections

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.

Topics: Animals; Anti-Infective Agents; Betaine; Chlorine; Chlorine Compounds; Collagen; Disinfectants; Fatty Acids, Unsaturated; Guinea Pigs; Oxides; Staphylococcal Infections; Surface-Active Agents; Surgical Wound Infection; Tensile Strength; Wound Healing

An anti-infective surfactant composition (C31G) promoted healing of infected and noninfected wounds in guinea pigs. In this animal model, histologic features of wounds treated topically with C31G revealed an increased rate of wound closure associated with decreased inflammatory response and increased C31G fibroblast infiltration and epithelialization. The effect of C31G on fibrin formation, the initial event of wound healing, was compared with effects of anionic and cationic surfactants that delay healing. The surfactants had different effects on clotting time, platelet activation, and cross-linkage of the stabilized clot. Seemingly, C31G increased the protein cross-linking of fibrin in clots containing fibronectin.

Topics: Animals; Betaine; Fatty Acids, Unsaturated; Guinea Pigs; Skin; Staphylococcal Infections; Surface-Active Agents; Wound Healing; Wounds, Penetrating