Abstract

Objective: to test the hypothesis that right atrial β-adrenoceptors are down-regulated after CPR and administration of β-adrenergic agents. Methods: after 3 min of ventricular fibrillation and 3 min of cardiac massage, 6 pigs received adrenaline (45 μg/kg) intravenously before defibrillation. After restoration of spontaneous circulation, dopamine was given in order to maintain the mean arterial blood pressure stable. Right atrial β-adrenergic binding sites were determined by an equilibration binding assay using (−)- 125Iodocyanopindolol. Results: plasma adrenaline (mean ± S.E.M.) was 1.1 ± 0.9 ng/ml (6.0 ± 4.9 nmol/l) pre-arrest and increased to 63.8 ± 45.8 (348.2 ± 250.0 nmol/l) ( P < 0.05) and 1034 ± 344 ng/ml (5644 ± 1878 nmol/l) ( P < 0.05) during CPR before and after adrenaline administration. At points in time 30 and 120 min after successful CPR, plasma adrenaline was 2.4 ± 0.5 and 1.3 ± 0.3 ng/ml (13.1 ± 2.7 and 7.1 ± 1.6 nmol/l). Compared to pre-arrest, the density of high-affinity β-adrenoceptors was 29.0 ± 12.8 fmol/mg pre-arrest and was 69.4 ± 21.6 and 84.2 ± 16.7 fmol/mg ( P < 0.05 vs. pre-arrest) 30 and 120 min after CPR. The density of low-affinity as well as of total binding sites was not significantly changed after CPR. Conclusions: it is concluded that markedly elevated plasma catecholamine concentrations after CPR and administration of adrenaline and dopamine do not lead to a decrease in the total density of β-adrenoceptors but to an increase in high-affinity β-adrenoceptors in right atrial cells.

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