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Effects of beta‐adrenoceptor antagonists on the pharmacokinetics of lignocaine.
Author(s) -
Tucker GT,
Bax ND,
Lennard MS,
AlAsady S,
Bharaj HS,
Woods HF
Publication year - 1984
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1984.tb02424.x
Subject(s) - propranolol , beta adrenoceptor , chemistry , in vivo , pharmacology , pharmacokinetics , adrenergic beta antagonists , beta (programming language) , free fraction , practolol , blood flow , adrenergic receptor , endocrinology , medicine , receptor , biochemistry , biology , microbiology and biotechnology , computer science , programming language
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.