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    Endogenous adenosine reduces depression of cardiac function induced by beta-adrenergic stimulation during low flow perfusion

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    Authors
    Fenton, Richard A.
    Galeckas, K. J.
    Dobson, James G. Jr.
    UMass Chan Affiliations
    Department of Physiology
    Document Type
    Journal Article
    Publication Date
    1995-10-01
    Keywords
    Adenosine
    Adrenergic beta-Agonists
    Animals
    Arrhythmias, Cardiac
    Coronary Circulation
    Epinephrine
    Isoproterenol
    Male
    Myocardial Contraction
    Myocardial Ischemia
    Myocardial Reperfusion Injury
    Perfusion
    Rats
    Rats, Sprague-Dawley
    Receptors, Adrenergic, beta
    Receptors, Purinergic P1
    Xanthines
    Cardiovascular Diseases
    Cellular and Molecular Physiology
    Physiology
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    Link to Full Text
    http://dx.doi.org/10.1016/S0022-2828(95)92055-2
    Abstract
    High levels of norepinephrine in the heart are cardiotoxic resulting in contractile dysfunction and arrhythmic activity via beta-adrenoceptor mediated mechanisms. A low flow heart model perfused with physiological saline containing glucose and bubbled with an O2 gas mixture was used to determine whether adenosine, a nucleoside with antiadrenergic properties, could reduce the functional manifestations of catecholamine cardiotoxicity. Isolated rat hearts were treated with dipropylcyclopentylxanthine (DPCPX; 0.1 microM; A1 receptor antagonist) to block endogenous adenosine. In DPCPX-treated hearts stimulated with isoproterenol (ISO; 1 microM) during 45 min of low flow (0.5 ml/min) perfusion, the recovery of contractile function (ConF) at 15 min after the restoration of normal flow was 64% of control (before low flow) values as compared to 110% recovery of ConF in the absence of ISO. The incidence of arrhythmias observed upon restoration of control flow was increased by ISO when the action of endogenous adenosine was blocked with DPCPX. In the absence of DPCPX both the functional depression and arrhythmias induced by ISO were prevented in the presence of phenylisopropyladenosine (PIA; 1 microM; A1 receptor agonist). At 15 min after normal flow was restored. ConF in ISO-treated hearts with PIA was 53% greater than in the absence of PIA and presence of DPCPX. This enhancement of ConF by PIA was significantly reduced by DPCPX. By 30 min after flow restoration, these significant differences were absent. DPCPX reversed the PIA-induced reduction in arrhythmias observed upon restoration of normal flow. PIA and DPCPX alone in the absence of ISO, and ISO in the absence of PIA and DPCPX, did not result in altered ConF upon restoration of normal flow. These findings indicate that intense beta-adrenergic stimulation of the heart during low-flow perfusion in the absence of adenosine A1 receptor activity induces contractile depression and arrhythmicity subsequent to restoration of control perfusion. It is concluded that endogenous adenosine protects the heart against catecholamine toxicity via stimulation of adenosine A1 receptors.
    Source
    J Mol Cell Cardiol. 1995 Oct;27(10):2373-83.
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/44170
    PubMed ID
    8576951
    Related Resources
    Link to article in PubMed
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    UMass Chan Faculty and Researcher Publications

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