Objective: to test the hypothesis that right atrial beta-adrenoceptors
are down-regulated after CPR and administration of beta-adrenergic ag
ents. Methods: after 3 min of ventricular fibrillation and 3 min of ca
rdiac massage, 6 pigs received adrenaline (45 mu g/kg) intravenously b
efore defibrillation. After restoration of spontaneous circulation, do
pamine was given in order to maintain the mean arterial blood pressure
stable. Right atrial beta-adrenergic binding sites were determined by
an equilibration binding assay using (-)-(125)Iodocyanopindolol. Resu
lts: 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 poi
nts 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 beta-adrenoce
ptors was 29.0 +/- 12.8 fmol/mg pre-arrest and was 69.4 +/- 21.6 and 8
4.2 +/- 16.7 fmol/mg (P < 0.05 vs. pre-arrest) 30 and 120 min after CP
R. The density of low-affinity as well as of total binding sites was n
ot significantly changed after CPR. Conclusions: it is concluded that
markedly elevated plasma catecholamine concentrations after CPR and ad
ministration of adrenaline and dopamine do not lead to a decrease in t
he total density of beta-adrenoceptors but to an increase in high-affi
nity beta-adrenoceptors in right atrial cells.