Regulation of postburn ischemia by α- and β-adrenoceptor subtypes

Deep skin burns are characterised by progressive ischemia secondary to vasoconstriction and thrombosis formation. Burn trauma elicits increased sympathetic activity and elevation of circulating catecholamines acting on adrenoceptors in vascular tissue playing an important role in the regulation of organ blood flow. The present study in rats investigated the role of α- and β-adrenoceptors in the circulatory changes taking place in normal skin and in partial- and full-thickness skin burns using laser Doppler flowmetry. Evaluation was based on intravenous administration of the following adrenergic agonists and antagonists: L-phenylephrine (α1-agonist), prazosin (α1-antagonist), clonidine (α2-agonist), yohimbine (α2-antagonist), prenalterol (β1-agonist), terbutaline (β2-agonist), and propranolol (β1- and β2-antagonist). Blood flow in normal skin was reduced by phenylephrine (p < 0.001), clonidine (p < 0.001) and propranolol (p < 0.01), and increased by prazosin (p < 0.05), yohimbine (p < 0.05), prenalterol (p < 0.05) and terbutaline (p < 0.01). In partial-thickness burns, blood flow was reduced by phenylephrine (p < 0.01), clonidine (p < 0.01) and propranolol (p < 0.05). In full-thickness burns, only clonidine reduced perfusion (p < 0.05). In conclusion, β1- and β2-adrenoceptors play important role in the physiological regulation of skin perfusion but are of lesser importance for postburn skin perfusion. Vasoconstrictive α1- and α2-adrenoceptors were shown to be tonically active in normal skin and in partial-thickness burns, exerting a negative effect on skin perfusion which was further potentiated by exogenous administration of α1- and α2-agonists and reversed by selective α-blockers. In full-thickness burns, activation of α2-receptors was shown to significantly impair skin circulation, raising a flag of warning for the use of clonidine to treat pain in burn patients.