Abstract

BackgroundPropofol may decrease myocardial contractility via actions on the β-adrenoceptor-mediated signal transduction. The aim of this study was to evaluate the effect of propofol via β-adrenoceptor-mediated signal transduction by measuring the tissue levels of cAMP (cyclic adenosine monophosphate).MethodsThe effects of propofol on β-adrenoceptor mediated cascades were measured with cAMP concentrations, which were stimulated by agonists (l-isoproterenol, GTPγS, and forskolin) of each step of β-adrenoceptor-mediated cascades.ResultsWhile the production of cAMP stimulated by isoproterenol, GTPγS, or forskolin are increased (P < 0.05), application of each concentration of propofol (0.1, 1, 10, 100 µM) did not alter the levels of cAMP.ConclusionsConsidering that propofol did not alter the tissue cAMP levels when stimulated by isoproterenol, GTPγS, and forskolin, propofol appears to have no effect on the β-adrenoceptor signaling pathway in guinea pig ventricular myocardium.

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