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British Journal of Clinical Pharmacology logoLink to British Journal of Clinical Pharmacology
. 1982 Mar;13(3):411–415. doi: 10.1111/j.1365-2125.1982.tb01394.x

On the role of alpha 1-acid glycoprotein in lignocaine accumulation following myocardial infarction.

A Barchowsky, D G Shand, W W Stargel, G S Wagner, P A Routledge
PMCID: PMC1402123  PMID: 7059443

Abstract

1 Blood plasma and free lignocaine concentrations have been measured 12 h after beginning a constant infusion of 2 mg/min and again at the end of the infusion (36-72 h) in five patients with myocardial infarction (MI) and compared with five control patients who did not develop objective evidence of MI. 2 In MI patients, total plasma concentration rose significantly between 12 h and the end of infusion. Because of an increase in alpha 1 acid glycoprotein (AAG) plasma binding increased, so that free drug concentration did not change. The rise in whole blood concentration was less than that in plasma as a result of drug redistribution out of red cells due to enhanced binding. 3 In control patients, neither blood nor plasma concentrations changed with time and plasma binding remained constant. Free drug concentrations, however, rose slightly. 4 The concentrations of GX and MEGX remained unchanged in all patients, but the ratio of lignocaine/MEGX concentrations fell in controls but rose in MI patients. 5 Pharmacokinetic modelling suggested that at least some of the rise in blood lignocaine concentration was due to reduced clearance resulting from enhanced plasma binding. 6 We conclude that the rise in AAG following MI is responsible for increased plasma binding and drug redistribution within blood. These changes, together with a reduction in lignocaine clearance, can explain much of the phenomenon of lignocaine accumulation in MI.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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