ABSTRACT
ABSTRACT. Background: Investigators have reported inter-patient variability with regard to propofol dosage for induction of anesthesia,since early dose finding studies. With the arrival of generic formulations of propofol, questions have arisen regarding furthervariability in dose requirements. Various studies have confirmed that generic propofol preparations are pharmacokineticallyand pharmacodynamically equivalent to Diprivan®. Nevertheless a number of practitioners are under the impression thatcertain generic propofol preparations require greater doses for induction of anaesthesia than does Diprivan®.Methods: 20 female patients of ASA status I-II, between the ages of 18-55 years, scheduled for routine surgery were randomlyallocated to two groups to undergo induction of anaesthesia using two different propofol formulations; Diprivan® andPropofol 1% Fresenius®. Either preparation was administered using a target-controlled infusion of propofol (STEL-TCI)targeting the plasma (central) compartment at a concentration of 6 µg.ml-1, employing the pharmacokinetic parameters ofMarsh et al. A processed EEG (bispectral index) was continuously recorded. Loss of consciousness (LOC) was regarded asthe moment at which the patient could not keep her eyes open and was confirmed by the absence of an eyelash reflex.At this point propofol administration was discontinued and data were recorded for a further two minutes, before administeringan appropriate opioid and/or nitrous oxide/volatile agent and/or muscle relaxant to maintain anaesthesia. Time to LOCafter start of propofol administration, and the dose of propofol administered during induction were annotated.Results: There were no demographic differences between the groups. There were no differences between the groups withregard to the mean dose for LOC, time to LOC and to the mean BIS values obtained at the following stages: awake, at LOC,at 1 and 2 minutes after LOC as well as the lowest recorded value.Conclusions: Our results confirm that the two propofol formulations that we studied, are pharmacologically equivalent withregard to induction of anaesthesia. Other mechanisms can explain the variability in clinical response to bolus administrationof propofol. The most important is the recirculatory or "front-end" kinetics of propofol in which cardiac output plays a majorrole, as well as the rate of drug administration. Emulsion degradation can also influence dose-response and in this regardit should be noted that the addition of foreign substances such as lignocaine, can result in rapid deterioration of the soya-bean emulsion