title: Progression of burn wound depth by systemical application of a vasoconstrictor: an experimental study with a new rabbit model.
abstract: The final depth of a necrosis resulting from burn trauma is determined within 3 days. The zone of stasis has the potential for complete regeneration or there may be ischemic influences that lead to necrosis. In our model, we examined the dermal influence of vasoconstrictors with reference to the development of burn necrosis. On the backs of New Zealand white rabbits (4.0-4.5 kg) standardized lesions were made with a heated aluminum stamp at 80 degrees C, 14 s in duration. The lesions were intradermal, whereby the border zone of the coagulated tissue was found in the middle two quarters of the dermis in 100% of untreated animals after 72 h. For dermal vasoconstriction epinephrine in a dose of 0.5 microg/kg/min was used. There were two groups of seven animals each. One group received epinephrine and the dosage was dependent on the clinical state of the animal. Several cycles were administered within a 3-day period. The reduction of skin perfusion was documented by Laser-Doppler-flowmetry. After 3 days, the skin with the lesions was excised and using a hematoxylin dye, a histological examination followed. The parameter used to determine the efficacy was the thickness of the uncoagulated part of the excised dermis. Over a period of 48 h, an average of 2.3 epinephrine cycles of average of 88 min per animal in duration resulted in an average reduction of skin diffusion of 41%. The uncoagulated part of the dermis in the epinephrine group was 28.6% average; in the control group, this was 43.5%. The statistical analysis revealed significant differences with a p-value of 0.0312 (significant, when value is less than 0.05). The test results indicate that temporary reduction of skin perfusion through external administration of vasocontrictors may lead to progression of burn necrosis in our animal model. Clinically, this result indicates that for patients with burn injuries and systemic inflammatory response syndrome who have insufficient volume therapy, the administration of vasocontrictors may produce similar results in the injured area.
authors.affiliation: Department of Surgery, University of Vienna-Medical School, AKH, Vienna, Austria.
authors.forename: J S
authors.initials: JS
authors.lastname: Knabl
authors.forename: W
authors.initials: W
authors.lastname: Bauer
authors.forename: H
authors.initials: H
authors.lastname: Andel
authors.forename: I
authors.initials: I
authors.lastname: Schwendenwein
authors.forename: P F
authors.initials: PF
authors.lastname: Dado
authors.forename: M
authors.initials: M
authors.lastname: Mittlböck
authors.forename: W
authors.initials: W
authors.lastname: Römer
authors.forename: M S
authors.initials: MS
authors.lastname: Choi
authors.forename: R
authors.initials: R
authors.lastname: Horvat
authors.forename: G
authors.initials: G
authors.lastname: Meissl
authors.forename: M
authors.initials: M
authors.lastname: Frey
mesh_terms: D000287:Administration, Topical; D000818:Animals; D002056:Burns / Q000188:drug therapy / Q000473:pathology*; D004195:Disease Models, Animal; D018450:Disease Progression; D004837:Epinephrine / Q000627:therapeutic use*; D017078:Laser-Doppler Flowmetry; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D009336:Necrosis; D011817:Rabbits; D012867:Skin / Q000098:blood supply / Q000293:injuries / Q000473:pathology*; D014662:Vasoconstrictor Agents / Q000627:therapeutic use*; D014945:Wound Healing / Q000187:drug effects*
chemical_list: D014662:Vasoconstrictor Agents; D004837:Epinephrine