This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Davis, P. J. Articles by Muir, K. T. Search for Related Content PubMed PubMed Citation Articles by Davis, P. J. Articles by Muir, K. T. Related Collections Blood Pharmacology

---

ANESTHETIC PHARMACOLOGY

In Vitro Remifentanil Metabolism: The Effects of Whole Blood Constituents and Plasma Butyrylcholinesterase

Peter J. Davis, MD^*, Richard L. Stiller, PhD^*, Annette S. Wilson, PhD^¶, Francis X. McGowan, MD^*#, Talmage D. Egan, MD, and Keith T. Muir, PhD^||

Departments of *Anesthesiology, Pediatrics, Pharmacology, and ¶Environmental and Occupational Health, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania; Department of Anesthesiology, University of Utah, School of Medicine, Salt Lake City, Utah; ||Clinical Pharmacokinetics, Glaxo-SmithKline; and #Department of Anesthesia, Harvard Medical School, Boston, Massachusetts

Address correspondence to Peter J. Davis, MD, Department of Anesthesiology, Children’s Hospital of Pittsburgh, 3705 5th Ave., Pittsburgh, PA 15213-2583. Address e-mail to davispj{at}anes upmc.edu.

We designed this in vitro study to determine whether the half-life of remifentanil was altered in butyrylcholinesterase-deficient patients. Test tubes containing Krebs buffered solution, whole blood, plasma, or red cells from both normal and butyrylcholinesterase-deficient patients were incubated with remifentanil. Remifentanil concentrations were determined by using gas chromatography and mean half-lives were calculated by using a nonlinear regression analysis. There were no differences in whole blood, red cells, or plasma half-life between normal and butyrylcholinesterase-deficient volunteers. In both normal and butyrylcholinesterase-deficient volunteers, whole blood and plasma had a significantly longer half-life than the red cell component. Extrapolation to the in vivo setting would suggest that a butyrylcholinesterase-deficient patient should not have altered remifentanil kinetics.

IMPLICATIONS: This was a test-tube-designed study to determine whether an enzyme deficiency (butyrylcholinesterase deficiency) changes the way remifentanil is metabolized. It seems that remifentanil dosage does not need to be changed in patients with butyrylcholinesterase deficiency.