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


Journal Article

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.

Full Text

Cited Authors

  • Barchowsky, A; Shand, DG; Stargel, WW; Wagner, GS; Routledge, PA

Published Date

  • March 1, 1982

Published In

Volume / Issue

  • 13 / 3

Start / End Page

  • 411 - 415

PubMed ID

  • 7059443

Pubmed Central ID

  • 7059443

Electronic International Standard Serial Number (EISSN)

  • 1365-2125

International Standard Serial Number (ISSN)

  • 0306-5251

Digital Object Identifier (DOI)

  • 10.1111/j.1365-2125.1982.tb01394.x


  • eng