title: Role of vasoactive intestinal polypeptide in burn-induced oedema formation.
abstract: Vasoactive intestinal polypeptide has been demonstrated to lack inherent effects on capillary permeability, but also to potentiate the oedema promoting actions of other inflammatory mediators or even to strongly reduce organ damage and subsequent oedema in ischemic models of the lung and heart. This study investigated the role of VIP on oedema in partial- and full-thickness skin burns of anaesthetised rats in vivo by spectrophotometrical quantification of Evans blue albumin. Results show that systemic VIP elicited a significant drop in mean arterial blood pressure versus saline (p<0. 001) and VIP antiserum (p<0.001) both in burned and non-burned animals. VIP also decreased heart rate versus saline (p<0.05) and anti-VIP (p<0.01) in non-burned and burned animals. EB-albumin in normal skin was significantly inhibited by VIP as compared to saline (p<0.05), but did not differ significantly from VIP-antiserum. A significant inhibition of EB-albumin extravasation versus saline was also seen following administration of VIP-antiserum (p<0.01). Similarly, VIP significantly reduced EB-albumin extravasation versus saline treatment in partial-thickness (p<0.01) and full-thickness burns (p<0.001), while VIP-antiserum had no significant effect on skin perfusion in any of the burned groups as compared to saline treatment. The present results show that systemic VIP is a potent inhibitor of burn oedema. This effect could be secondary to constriction of skin vessels as a result of VIP-induced systemic hypotension or be mediated by the interaction of VIP with other oedema promoting mediators released following a thermal trauma to the skin.
authors.affiliation: Department of Physiology & Pharmacology, Göteborg University, Sweden.
authors.forename: L
authors.initials: L
authors.lastname: Lindblom
authors.forename: J
authors.initials: J
authors.lastname: Cassuto
authors.forename: L
authors.initials: L
authors.lastname: Yregård
authors.forename: P
authors.initials: P
authors.lastname: Tarnow
authors.forename: J
authors.initials: J
authors.lastname: Räntfors
authors.forename: P
authors.initials: P
authors.lastname: Löwhagen Hendén
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002056:Burns / Q000503:physiopathology*; D002199:Capillary Permeability / Q000187:drug effects; D004396:Coloring Agents; D004487:Edema / Q000209:etiology* / Q000503:physiopathology; D005070:Evans Blue; D005119:Extravasation of Diagnostic and Therapeutic Materials / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D007022:Hypotension / Q000503:physiopathology; D007106:Immune Sera / Q000494:pharmacology; D018836:Inflammation Mediators / Q000502:physiology; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012867:Skin / Q000098:blood supply / Q000187:drug effects / Q000293:injuries; D012871:Skin Diseases / Q000209:etiology* / Q000503:physiopathology; D012965:Sodium Chloride; D013053:Spectrophotometry; D014660:Vasoactive Intestinal Peptide / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000037:antagonists & inhibitors / Q000494:pharmacology*
chemical_list: D004396:Coloring Agents; D007106:Immune Sera; D018836:Inflammation Mediators; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D014660:Vasoactive Intestinal Peptide; D012965:Sodium Chloride; D005070:Evans Blue