| Objective To investigate the effect of acute hypervolemic hemodilution (AHHD) on plasma propofol concentrations and performance of target-controlled infusion (TCI) and relationship between the concentrations of propofol and the changes of hemodynamics, and the time of lost consciousness during TCI. Methods Seventy-nine patients, ASA I - II, scheduled for operations were randomly divided into two groups. Lactated Ringer's solution (10 ml/kg) were administrated in both groups during TCI. The AHHD group was performed AHHD by 6% HES (20ml/kg) and Lactated Ringer's solution (10ml/kg) as soon as TCI started and the control group did not. Radial artery was cannulated for MAP monitoring and blood sampling. Anesthesia was induced and maintained with propofol, with a single constant target plasma propofol concentration of 3ug/ml. When the patients lost consciousness, a loading dose of fentanyl 2ug/kg and vecuronium 0.1mg/kg were given followed by 2ug/kg. When muscle paralysis was satisfied the trachea was intubated. The TCI system consisted of a computer, a Graseby 3500 infusion pump, Stelpump software (Version 1.07 by JF Coetzee and R Pina), and the pharmacokinetic model and parameter by Tackley et al. Blood samples were obtained before and 2-60min during and 30min after propofol TCI for determination of blood propofol concentration by Gas Chromatography-Mass Spectrometry (GC-MS). The MAP and HR were monitored and recorded the time of lost of consciousness during anesthesia. Results Compared with basic levels, after AHHD Hb and Hct dropped by 30.8% and 31.3%, respectively. The measured propofolconcentrations of the test group were significantly lower than control group at different time-site during TCI (P<0.05) and the biggest drop was 38.5% at the end of AHHD. During AHHD, median performance error (MDPE) and median absolute performance error (MDAPE) were -27.18% and 27.18%, respectively. The time of lost of consciousness in control group was (2.01±0.53)min; It took 2min to reach the peak of concentration and with the time passing by the concentration gradually declined closely to the target; When the propofol concentration was more than 4.59ng/ml, MAP declined by 22.1% from the basic value (93.0±10.2) mmHg to (72.5±11-7) mmHg; otherwise, MAP was gradually up to (80.2±11.2)mmHg, below the base line of 14%; When propofol concentration was more than 3.73μg/ml, HR declined by 15.5% from the basic value (89.2±13.6) b/min to (75.4± 12.1) b/min, otherwise, HR rose gradually to (77.9±13.8) b/min, below the base line 13.5% ; Conclusions The performance of TCI system in two groups using pharmacokinetic parameters from Tackley were beyond the normal range (15% and 30%, respectively), with the system of TCI overestimated firstly and then lowerestimated significantly the measured concentrations. Acute moderate hemodilution resulted in significantly lower of the measured concentrations than control group, resulted from the larger central compartment volume and faster clearance rate during AHHD than in normal situation. Target concentration of 3μg/ml could be supplied satisfactory sedation and good conditions of trachea intubation; Propofol concentration was unrelated to hemodynamics during TCI.
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