British Journal of Anaesthesia, Vol 82, Issue 1 38-40, Copyright © 1999 by The Board of Management and Trustees of the British Journal of Anaesthesia
E. Hammaren, P. H. Rosenberg and M. Hynynen
Propofol is sequestered in extracorporeal circuits, but the factors
responsible for the phenomenon are mostly unknown. We have compared two
extracorporeal circuits (oxygenators, reservoirs and tubings) coated with
heparin with two corresponding uncoated circuits for their capacity to
sequester propofol in vitro. Three experiments were conducted with each
circuit. The circuit was primed with a mixture of Ringer's acetate solution
and whole blood, and the study conditions (pump flow, temperature, pH) were
standardized. Propofol was added to the solution to achieve a concentration
of 2 micrograms ml-1. These studies were followed with concentrations of
10- and 100-fold to assess possible saturation of propofol binding. Serial
samples were obtained from the circulating solution for measurement of
propofol concentration. Propofol concentrations decreased to 22-32% of the
initial predicted concentration of 2 micrograms ml-1 in the circuits (no
significant difference between circuits). With greater concentrations, the
circuits did not become saturated with propofol, even with the highest
predicted concentration of 200 micrograms ml-1. We conclude that propofol
was sequestered in extracorporeal circuits in vitro, irrespective of
coating the circuit with heparin.
CLINICAL INVESTIGATIONS
Coating of extracorporeal circuit with heparin does not prevent sequestration of propofol in vitro
Department of Anaesthesia, Helsinki University Hospital, Haartmaninkatu 4, FIN-00290 Helsinki, Finland. Department of Anaesthesia and Intensive Care, Jorvi Hospital, Turuntie 150, FIN-02740 Espoo, Finland
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