title: [Microvascular effects of burn plasma transfer and therapeutic options in a rat model].
abstract: BACKGROUND
  Thermal injuries with more than 20% of burned body surface area (BSA) lead to systemic shock with generalised oedema in addition to local tissue destruction. This condition, known as burn injury, is caused by immunmodulative mediators whose individual significance is not known in detail. We present an experimental model where plasma of burned animals (burn plasma) is transmitted to healthy animals, to trigger burn iniury without performing direct burn trauma.
  
  
  METHODS
  The systemic oedema is measured by extravasation of fluorescent albumin in mesenterial venules of Wistar rats. In addition, leukocyte-endothelial interactions ("leukocyte rolling and sticking") is examined.
  
  
  RESULTS
  The systemic capillary leak is induced by both direct thermal trauma as well as by infusion of burn plasma. This is evident even after plasma dilution (1% in Ringer's lactate) of the burn plasma. In addition, topical therapy for burned animals (donors) with cerium nitrate led to a significant reduction of plasma extravasation in receiver animals. In addition, systemic antioxidant therapy with high-dose vitamin C of receiver animals, led to a significant reduction of the capillary leak. Leukocyte-endothelial interactions are not significantly affected in either case.
  
  
  CONCLUSIONS
  In summary, for the first time a reliable model of burn injury has been established, which eliminates mediator-independent effects. In addition, our studies show that antioxidant therapy with high doses of vitamin C and topical treatment with cerium nitrate both reduce the systemic capillary leak in receiver animals. Their positive influence could therefore soon be integrated in clinical treatment algorithms.
authors.affiliation: BG Unfallklinik Ludwigshafen, Klinik für Hand-, Plastische- und Rekonstruktive Chirurgie-Schwerbrandverletztenzentrum, Ludwigshafen.
authors.forename: J F
authors.initials: JF
authors.lastname: Hernekamp
authors.forename: P S
authors.initials: PS
authors.lastname: Harenberg
authors.forename: M
authors.initials: M
authors.lastname: Lehnhardt
authors.forename: G
authors.initials: G
authors.lastname: Germann
authors.forename: A
authors.initials: A
authors.lastname: Walther
authors.forename: T
authors.initials: T
authors.lastname: Kremer
mesh_terms: D000818:Animals; D000891:Anti-Infective Agents, Local / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D001205:Ascorbic Acid / Q000494:pharmacology; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D002056:Burns / Q000188:drug therapy / Q000276:immunology*; D019559:Capillary Leak Syndrome / Q000188:drug therapy / Q000276:immunology*; D002448:Cell Adhesion / Q000187:drug effects / Q000276:immunology*; D002563:Cerium / Q000494:pharmacology; D016207:Cytokines / Q000502:physiology*; D004195:Disease Models, Animal; D004487:Edema / Q000276:immunology*; D005119:Extravasation of Diagnostic and Therapeutic Materials; D007962:Leukocytes / Q000187:drug effects / Q000276:immunology*; D008297:Male; D008642:Mesenteric Veins / Q000187:drug effects / Q000276:immunology; D008833:Microcirculation / Q000187:drug effects / Q000276:immunology*; D010949:Plasma / Q000276:immunology*; D051381:Rats; D017208:Rats, Wistar; D012769:Shock / Q000188:drug therapy / Q000276:immunology*; D014699:Venules / Q000187:drug effects / Q000276:immunology
chemical_list: D000891:Anti-Infective Agents, Local; D000975:Antioxidants; D016207:Cytokines; C032786:cerium nitrate; D002563:Cerium; D001205:Ascorbic Acid