title: Influence of anti-inflammatory and vasoactive drugs on microcirculation and angiogenesis after burn in mice.
abstract: OBJECTIVE
  The treatment of burns remains a challenge. Besides the administration of physiological saline, local disinfection and symptomatic medications, no causal therapy is known to accelerate angiogenesis and wound healing. The aim of this study was to investigate the influences of dilatative and anti-inflammatory acting drugs on microcirculation, angiogenesis and leukocyte behavior, which had shown positive effects in former burn studies.
  
  
  METHODS
  The ears of male hairless mice (n=47) were inflicted with full thickness burns using a hot air jet. Then the affects of five intraperitoneal injections of either acetylsalicylic acid (ASA), isosorbide dinitrate, prostaglandin E1 (PGE1) or sodium chloride (each administered to one of four corresponding study groups), on microcirculation, leukocyte-endothelial interaction and angiogenesis were investigated over a 12 day period using intravital fluorescent microscopy.
  
  
  RESULTS
  Angiogenesis was slightly improved by PGE1 (0.3 vs. 1.3% non-perfused area in other groups on day 12, p=0.029). Additionally, blood flow increased and rolling leukocytes decreased compared to other groups. The ASA-group showed best functional vessel density and lowest leukocyte-adhesion. The often described posttraumatic expansion of tissue damage could not be observed in either group.
  
  
  CONCLUSIONS
  Prostaglandin E1 improved angiogenesis, increased the blood flow and reduced the number of rolling leukocytes. ASA had positive influences on functional vessel density, edema formation and the number of sticking leukocytes. However, it reduced the blood flow. Overall, out of all the drugs tested, prostaglandin seems to have the greatest positive impact on microcirculation and angiogenesis in burns.
authors.affiliation: Department of Plastic and Hand Surgery, Burn Center, BG-University Hospital Bergmannsheil, Ruhr-University Bochum, Bochum, Germany. ole.goertz@rub.de
authors.forename: O
authors.initials: O
authors.lastname: Goertz
authors.forename: A
authors.initials: A
authors.lastname: Ring
authors.forename: B
authors.initials: B
authors.lastname: Buschhaus
authors.forename: T
authors.initials: T
authors.lastname: Hirsch
authors.forename: A
authors.initials: A
authors.lastname: Daigeler
authors.forename: L
authors.initials: L
authors.lastname: Steinstraesser
authors.forename: H-U
authors.initials: HU
authors.lastname: Steinau
authors.forename: S
authors.initials: S
authors.lastname: Langer
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001241:Aspirin / Q000031:analogs & derivatives / Q000494:pharmacology; D002056:Burns / Q000188:drug therapy* / Q000503:physiopathology; D004195:Disease Models, Animal; D004727:Endothelium / Q000473:pathology; D007274:Injections, Intraperitoneal; D007547:Isosorbide / Q000031:analogs & derivatives / Q000494:pharmacology; D007962:Leukocytes / Q000473:pathology; D051379:Mice; D008812:Mice, Hairless; D008833:Microcirculation / Q000187:drug effects*; D009389:Neovascularization, Pathologic / Q000188:drug therapy*; D011453:Prostaglandins / Q000494:pharmacology; D012867:Skin / Q000098:blood supply* / Q000473:pathology; D012965:Sodium Chloride / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D000893:Anti-Inflammatory Agents; D011453:Prostaglandins; D014665:Vasodilator Agents; C473019:isosorbide diaspirinate; D012965:Sodium Chloride; D001241:Aspirin; D007547:Isosorbide