Circulation, Vol 87, 422-426, Copyright © 1993 by American Heart Association
D Schranz, A Droege, A Broede, G Brodermann, E Schafer, H Oelert and OE Brodde
BACKGROUND. It is well known that during cardiopulmonary bypass (CPB) with
cardioplegic cardiac arrest, catecholamines are vigorously increased. We
therefore investigated whether this might cause desensitization of human
cardiac beta-adrenoceptors. METHODS AND RESULTS. We assessed in 12 children
with acyanotic congenital heart disease who underwent open-heart surgery
right atrial beta-adrenoceptor number and subtype distribution [by
(-)-[125I]iodocyanopindolol binding] and adenylate cyclase activation [by
the beta-adrenoceptor agonist isoprenaline (100 microM) and by the
non-receptor-mediated activators 10 microM GTP, 10 mM NaF, 100 microM
forskolin, and 10 mM Mn2+] before and after CPB with cardiac arrest by
means of St. Thomas' cardioplegic solution. CPB affected neither
beta-adrenoceptor number of subtype distribution nor GTP-, NaF-,
forskolin-, or Mn(2+)-induced activation of adenylate cyclase. In contrast,
activation of adenylate cyclase by 100 microM isoprenaline was
significantly (p = 0.0249) lower after CPB than before CPB. CONCLUSIONS.
CPB with cardioplegic cardiac arrest decreases beta-adrenoceptor-mediated
adenylate cyclase activation in a manner compatible with an uncoupling of
beta- adrenoceptors from the Gs-protein-adenylate cyclase complex. Such a
beta-adrenoceptor desensitization may be the reason why after CPB many
patients need inotropic support but do not respond sufficiently to
catecholamines.
ARTICLES
Uncoupling of human cardiac beta-adrenoceptors during cardiopulmonary bypass with cardioplegic cardiac arrest
Department of Internal Medicine, University of Essen, FRG.
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