Objectives: Cardiac dysfunction following brain death is associated with highly increased myocardial norepinephrine, lactate and adenosine concentrations. Administration of labetalol, a mixed a-, 13-adrenergic receptor antagonist, attenuates metabolic disturbances and improves myocardial function. The purpose of this study was to investigate p-adrenergic receptor (f3AR)density and affinity in the presence or absence of labetalol administration, as a possible mechanism of the protective effects of this drug. Methods: Experimental animals were divided into three groups: sham-operated, brain-dead pigs, and brain-dead pigs treated with labetalol (10 mg/kg). The maximum number of binding sites (Bmax) and the dissociation constant (Kd) of pAR were determined with(-) [125^I]cyanopindololon myocardial samples harvested 3 hours after brain death. Results: Left ventricular pAR density and affinity were identical in brain-dead and sham-operated animals. Labetalol-treated pigs exhibited a significant decrease of Bmax and an increase of Kdas compared with brain-dead pigs. Bmax decrease was due to the persistence of labetalol in the membrane preparations. Increased Kd was too low to be biologically significant. Therefore, pAR number and affinity can be considered as unchanged after adrenergic blockade with labetalol. Conclusions:The protective mechanism of labetalol on brain death-induced myocardial dysfunction cannot be explained by changes in pAR density and affinity but is probably related to a preservation of the oxygen consumption/oxygen delivery balance during the autonomic storm.

Keywords: Brain Death, beta-adrenergic receptor, adrenergic receptors antagonists, radioligand binding