Open AccessFunctional Characterization of an Ex Vivo Preparation of Atrial Myocardium from Children with Congenital Heart Defects
Author(s) -
Kjell Borthne,
P Hågå,
A Langslet,
Harald Lindberg,
JanBjørn Osnes,
Tor Skomedal
Publication year - 1994
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-199409000-00003
Subject(s) - inotrope , medicine , prazosin , tyramine , contractility , endocrinology , stimulation , antagonist , propranolol , adrenergic , endogeny , basal (medicine) , chronotropic , isometric exercise , timolol , chemistry , heart rate , receptor , blood pressure , surgery , intraocular pressure , insulin
Small pieces of atrial tissue removed from the cannulation site before cardioplegia were used to develop a method for studying adrenergic regulation of the myocardial contractile force in children operated on for congenital heart defects (CHD). We measured the development of the isometric force of contraction dT/dtmax (T'max). Reduction in basal contractility induced by the beta-adrenoceptor antagonist timolol indicated that the myocardium was about half-maximally stimulated by endogenous norepinephrine (NE), probably released from nerve endings by the electrical stimulation. The inotropic effect of endogenous NE could be further increased by tyramine (EC50 approximately 5 microM). A maximal concentration of tyramine increased T'max by a median of 62.5% above the basal level. Sequential blockade of the beta- and alpha 1-adrenoceptors after tyramine stimulation by timolol and prazosin, respectively, indicated that a near-maximal response to combined adrenoceptor stimulation by endogenous NE was mediated by both beta-adrenoceptors (median 77%) and alpha 1-adrenoceptors (median 23%). The basal level of endogenous NE may conceal inotropic effects by exogenous alpha-agonists added to this type of preparation. This preparation is suitable for studying adrenergic regulation by reversing the effects of endogenous NE.