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  • Title: Halothane effect on beta-adrenergic receptors in canine myocardium.
    Author: Bernstein KJ, Gangat Y, Verosky M, Vulliemoz Y, Triner L.
    Journal: Anesth Analg; 1981 Jun; 60(6):401-5. PubMed ID: 6263132.
    Abstract:
    Halothane depresses the inotropic state of the heart, possibly by decreasing the rate of formation of cyclic 3',5'-adenosine monophosphate (cAMP) through depression of the activity of adenylate cyclase, the cAMP-generating enzyme. As catecholamines regulate the inotropic state and adenylate cyclase activity by binding to myocardial beta-adrenergic receptors, the effect of halothane on binding to these receptors was studied to determine whether this was a site of halothane effect. Beta-adrenergic binding was measured at binding equilibrium in vitro in a canine myocardial membrane preparation in the absence and presence of halothane, 3 to 5 vol%, using as the radioligand 3H-dihydroalprenolol (3H-DHA), a beta-adrenergic antagonist with high affinity and radioactivity. In addition, the effect of halothane on the binding of l-isoproterenol, a beta-adrenergic agonist, was measured by displacement of 3H-DHA. The results indicate that halothane has no effect on either the affinity of canine myocardial beta-adrenergic receptors for 3H-DHA or l-isoproterenol, nor does it alter the number of available receptors at binding equilibrium.
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