Thomas Thurston

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The involvement of the adenylate cyclase system in myocardial depression by halothane was investigated in an isolated, electrically stimulated, rat left atrial preparation. The twitch tension dose-response curve to the muscarinic agent, carbachol, was unaltered by 0.27 mM (0.8%) halothane. Pertussis toxin irreversibly blocks the inhibition of adenylate(More)
Depression of myocardial contractility by muscarinic agonists is dependent on underlying beta-adrenergic tone. The negative inotropic effect of muscarinic agonists is enhanced by previous beta-adrenergic stimulation, an action that has been termed accentuated antagonism. We wished to determine whether accentuated antagonism occurs with isoflurane-induced(More)
The purpose of this study was to determine the importance of inhibition of beta-adrenergic function in thiopentone-induced myocardial depression. Using an isolated, electrically stimulated rat left atria model, contractile dose-response curves to thiopentone (200 microM, 400 microM, 600 microM, 800 microM) were shifted to the right in preparations treated(More)
BACKGROUND Depression of myocardial contractility by muscarinic stimulation is dependent on the underlying beta-adrenergic tone. Prior beta-adrenergic stimulation enhances muscarinic negative inotropic responses, an effect that has been termed accentuated antagonism. The purpose of this study was to determine whether accentuated antagonism occurs with(More)
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