Propofol does not appear to decrease myocardial contractility via the beta-adrenoceptor signaling pathway, as it does not alter cAMP levels in guinea pig ventricular myocardium.
Propofol's myocardial effects unlikely via beta-adrenoceptor cAMP pathway in guinea pigs; leaves open alternative mechanisms for investigation.
BACKGROUND: Propofol may decrease myocardial contractility via actions on the beta-adrenoceptor-mediated signal transduction. The aim of this study was to evaluate the effect of propofol via beta-adrenoceptor-mediated signal transduction by measuring the tissue levels of cAMP (cyclic adenosine monophosphate). METHODS: The effects of propofol on beta-adrenoceptor mediated cascades were measured with cAMP concentrations, which were stimulated by agonists (l-isoproterenol, GTPgammaS, and forskolin) of each step of beta-adrenoceptor-mediated cascades. RESULTS: While the production of cAMP stimulated by isoproterenol, GTPgammaS, or forskolin are increased (P < 0.05), application of each concentration of propofol (0.1, 1, 10, 100 microM) did not alter the levels of cAMP. CONCLUSIONS: Considering that propofol did not alter the tissue cAMP levels when stimulated by isoproterenol, GTPgammaS, and forskolin, propofol appears to have no effect on the beta-adrenoceptor signaling pathway in guinea pig ventricular myocardium.
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Chang et al. (2010) studied this question.
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