title: Adrenoceptor subtypes in the control of burn-induced plasma extravasation.
abstract: Burn trauma is known to induce a significant rise in circulating catecholamine levels and despite catecholamines being potent endogenous vasoactive agents with known actions on microvascular permeability, their effect on burn edema has been poorly investigated. The present study in rats investigated the role and importance of adrenergic receptor subtypes in the regulation of basal capillary permeability in normal skin and hyperpermeability in partial- and full-thickness skin burns. Edema was quantified by spectrophotometric analysis of extravasated Evans blue-albumin. Evaluation was based on intravenous administration of the following adrenergic agonists and antagonists: l-phenylephrine (alpha(1)-receptor agonist), prazosin (alpha(1)-receptor antagonist), clonidine (alpha(2)-receptor agonist), yohimbine (alpha(2)-receptor antagonist), prenalterol (beta(1)-receptor agonist), terbutaline (beta(2)-receptor agonist), or propranolol (beta(1)- and beta(2)-receptor antagonist). Results showed increased capillary permeability in normal skin following administration of terbutaline (p<0.01) and yohimbine (p<0.01). In partial-thickness burns, clonidine significantly (p<0.05) reduced edema formation, whereas in full-thickness burns edema was significantly reduced by clonidine (p<0.05) and l-phenylephrine (p<0.01). In conclusion, the inhibition of postburn edema induced by stimulation of alpha(1)-receptors (l-phylephrine) and alpha(2)-receptors (clonidine) could be secondary to increased vascular resistance and reduced tissue perfusion pressure and/or suppressed inflammatory reaction in the burn injury. In the treatment of burn patients, clonidine is particularly interesting since the agent has previously been proven to induce potent analgesia in thermally injured.
authors.affiliation: Department of Anaesthesia and Intensive Care and Institution of Surgical Specialties, Sahlgrenska University Hospital, Mölndal, Sweden. jean.cassuto@aniv.gu.se
authors.forename: Jean
authors.initials: J
authors.lastname: Cassuto
authors.forename: Peter
authors.initials: P
authors.lastname: Tarnow
authors.forename: Liselotte
authors.initials: L
authors.lastname: Yregård
authors.forename: Lucky
authors.initials: L
authors.lastname: Lindblom
authors.forename: Johanna
authors.initials: J
authors.lastname: Räntfors
mesh_terms: D000322:Adrenergic Agonists / Q000008:administration & dosage; D018674:Adrenergic Antagonists / Q000008:administration & dosage; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002056:Burns / Q000378:metabolism / Q000503:physiopathology*; D002199:Capillary Permeability / Q000187:drug effects / Q000502:physiology*; D004487:Edema / Q000503:physiopathology / Q000517:prevention & control; D006339:Heart Rate / Q000502:physiology; D007262:Infusions, Intravenous; D007275:Injections, Intravenous; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D011941:Receptors, Adrenergic / Q000378:metabolism*; D012867:Skin / Q000187:drug effects / Q000378:metabolism*
chemical_list: D000322:Adrenergic Agonists; D018674:Adrenergic Antagonists; D011941:Receptors, Adrenergic