The therapeutic effect of C1-inhibitor on gut-derived bacterial translocation after thermal injury.

To test the effects of C1-esterase inhibitor in scald burns on bacterial translocation and intestinal damage, standardized deep partial-thickness burns were inflicted on domestic pigs, scalding 30% of the skin surface for 25 s with 75 degrees C hot water. The animals (n = 17; weight 25-35 kg) were divided into three groups: I) the control group (n = 5) without scald burn; II) the group (n = 6) with scald burn; and III) the group with C1-inhibitor (n = 6): scald burn and treatment with C1-inhibitor (C1-INH; BERINERT, Behring, Marburg, Germany). Parameters measured and compared in this model were activity of complement system, hemodynamics, body weight, pathological organ alterations including intestinal lesions, bacterial translocation, and skin damage. C1-INH administration significantly decreased the plasma levels of the specific soluble membrane attack complex (SC5b-9), bacterial translocation, and the degree of intestinal ischemia in the postburn period compared with untreated animals. Moreover, animals treated with C1-INH exhibited a minor degree of organ alterations including damage of the skin and development of edema. The favorable effects of C1-INH may be explained by the protection of the intestinal and dermal microcirculation in the acute phase of thermal injury.

The influence of the C1-inhibitor BERINERT and the protein-free haemodialysate ACTIHAEMYL20% on the evolution of the depth of scald burns in a porcine model.

Standardized deep partial-thickness burns were inflicted on domestic pigs by scalding 30 per cent of the skin surface for 25 s with 75 degrees C hot water. The animals (n = 18; weight 25-35 kg) were divided into three groups: I, control group (n = 6), Ringer's lactate only; II, haemodialysate group (n = 6), Ringer's lactate and a protein-free haemodialysate of calf-blood (ACTIHAEMYL20%; AH) and III, C1-inhibitor group (n = 6), Ringer's lactate and C1-inhibitor (C1-INH; BERINERT). Skin biopsies were taken at defined time points (4, 28, 52 and 76 h) and investigated histologically. Depth of burn was determined morphometrically after coloration with a modified MTT-staining on frozen sections of the skin biopsies. Fluid therapy with C1-INH decelerated significantly the progression of the burn wound in the postburn-period compared to Ringer's lactate alone. In comparison with C1-INH, the treatment with AH demonstrated a less beneficial influence on the depth of scald burns. The favourable effects of C1-INH are explained by the protection of the dermal microcirculation during the acute phase of thermal injury.