Effects of beta-adrenoceptor antagonists on the pharmacokinetics of lignocaine.
In theory, beta-adrenoceptor antagonists could lower the clearance of free lignocaine in three ways (a) by decreasing hepatic blood flow, (b) by competing for plasma binding sites or (c) by inhibiting the enzymes responsible for metabolising lignocaine. The first mechanism has been demonstrated for propranolol and is probably common to all agents lacking intrinsic sympathomimetic activity. The second mechanism is discounted by data showing that propranolol, one of the more highly bound beta-adrenoceptor antagonists, does not alter the free fraction of lignocaine in plasma. In vitro studies support the third mechanism for the more lipid-soluble beta-adrenoceptor antagonists, as does the fact that observed decreases in the clearance of lignocaine in vivo are generally greater than the anticipated maximum lowering of hepatic blood flow.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D001798:Blood Proteins / Q000378:metabolism; D004347:Drug Interactions; D006801:Humans; D007275:Injections, Intravenous; D007700:Kinetics; D008012:Lidocaine / Q000378:metabolism*; D008102:Liver Circulation / Q000187:drug effects; D008954:Models, Biological; D011485:Protein Binding
D000319:Adrenergic beta-Antagonists; D001798:Blood Proteins; D008012:Lidocaine