title: Importance of vasoactive intestinal polypeptide in the regulation of burn perfusion.
abstract: Vasoactive intestinal polypeptide is one of the body's most potent vasodilators and has been shown to increase blood flow in a number of tissues. Its effects on postburn skin perfusion and progressive ischemia was investigated in rats exposed to partial- and full-thickness experimental skin burns. Systemic administration of 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 nonburned animals. VIP also decreased heart rate versus saline (p<0.05) and anti-VIP (p<0.001) in nonburned and burned animals. In contrast, VIP antiserum significantly increased blood pressure (p<0. 001) and heart rate (p<0.001) versus saline in all the groups. Skin perfusion in normal skin was significantly impaired by VIP infusions as compared to saline (p<0.01) while VIP-antiserum did not differ significantly from saline. Similarly, VIP significantly reduced blood flow versus saline-treatment in partial-thickness (p<0.01) and full-thickness burns (p<0.05) 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 VIP is directly involved in general cardiovascular control but plays a minor role in the maintenance of skin perfusion following a thermal injury as suggested by the lack of effect of VIP-antiserum. In contrast, exogenous administration of VIP significantly and dramatically impaired skin perfusion in normal and burned skin probably by increasing blood flow in organs of higher priority such as the brain and heart and concomitantly inducing a pronounced vasoconstriction in the skin, probably as a result of increased sympathetic effect on peripheral organs in order to maintain blood pressure.
authors.affiliation: Department of Physiology and 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: D000704:Analysis of Variance; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002056:Burns / Q000145:classification / Q000503:physiopathology*; D002320:Cardiovascular Physiological Phenomena / Q000187:drug effects; D016001:Confidence Intervals; D006339:Heart Rate / Q000187:drug effects; D007106:Immune Sera / Q000494:pharmacology; D007511:Ischemia / Q000503:physiopathology; D017078:Laser-Doppler Flowmetry; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow / Q000187:drug effects; D012867:Skin / Q000098:blood supply* / Q000293:injuries; D012965:Sodium Chloride; D013564:Sympathetic Nervous System / Q000187:drug effects; D014660:Vasoactive Intestinal Peptide / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D014665:Vasodilator Agents / Q000037:antagonists & inhibitors / Q000494:pharmacology*
chemical_list: D007106:Immune Sera; D014665:Vasodilator Agents; D014660:Vasoactive Intestinal Peptide; D012965:Sodium Chloride