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PubMed2004

Dexmedetomidine vs. propofol for short-term sedation of postoperative mechanically ventilated patients.

BACKGROUND: Propofol is often used for sedation in the intensive care unit. The aim of this study was to compare the efficacy and endocrine response of propofol vs. the new alpha2-agonist dexmedetomidine for sedation in surgical intensive care patients who need postoperative short-term ventilation. METHODS: Our work is a randomized clinical study conducted on sixty adult patients who required postoperative short term ventilation and sedation. The patients were allocated randomly, to receive IV infusion of either dexmedetomidine 0.2-0.5 microg/kg/h or propofol 0.5-1 mg/kg/h. Hemodynamic parameters, Ramsay sedation score, extubation time and serum cortisol and interleukin-6 (IL-6) levels were measured. RESULTS: Ramsay sedation score was 4.1+/-1 and 4+/-0.9 for propofol and dexmedetomidine, respectively, (p=0.59.) Total fentanyl dose in the propofol group was 75+/-15 microg compared to 15+/-10.5 microg in the dexmedetomidine group, (p=0.0045). Patients who received dexmedetomidine infusion had significantly lower heart rates compared to patients who received propofol infusion, (p=0.041). Pre-infusion serum concentrations of IL-6 were comparable in both groups, while the 24 h post-infusion levels were insignificantly decreased in both groups compared to pre-infusion level, (p=0.36). There were no intergroup differences in serum cortisol concentrations (p=0.231). CONCLUSIONS: Dexmedetomidine and propofol are safe sedative drugs for postoperative mechanichally ventilated patients. Patients were easily aroused to co-operate without showing signs of irritations with less fentanyl analgesia in the dexmedetomidine group. Dexmedetomidine and propofol do not inhibit adrenal function, but they may influence the inflammatory response.

Journal Article↗
PubMed2003

HPLC investigation of free and bound propofol in human plasma and cerebrospinal fluid.

The paper compares the total propofol concentration in the cerebrospinal fluid (CSF) with the free drug concentration in plasma measured in 35 humans scheduled for elective neurosurgical procedures during propofol anaesthesia. The concentrations of total and free propofol in the blood and CSF samples were measured by means of HPLC using liquid-liquid extraction and ultrafiltration in the sample preparation procedure. The arterial blood and CSF samples (collected from intraventricular drainage) were taken at the same time. According to the obtained results, the usually expected equality between free drug concentration in plasma and its total concentration in CSF is not valid for propofol: the unbound propofol concentration in plasma is not equal to its total concentration in CSF (p < 0.05). This difference suggests a substantial contribution of active transport in propofol transfer from blood into CSF. Moreover, the paper shows the presence of bound propofol in CSF, which is a novel finding.

Anesthetics, Intravenous↗
PubMed2001

The influence of blood sample storage time on the propofol concentration in plasma and solid blood elements.

In order to describe the changes of propofol concentration in whole blood and in its components during the blood storage we examined venous blood samples collected from patients anaesthetized either with or without propofol. Blood samples from patients anaesthetized without propofol were spike with propofol 45 min before analysis. Propofol concentration was examined in whole blood, plasma, rinsed formed elements and rinsed and lysed formed blood elements by means of HPLC after 1, 4, 7, 13, 21, 25 and 28 days of storage. There was significant decrease in plasma concentration of propofol during the first few days of sample storage followed by its increase during subsequent days. The opposite phenomenon was observed for formed blood elements. The findings support the hypothesis that propofol distribution between blood components changes in time.

Anesthetics, Intravenous↗
PubMed2003

The influence of endotoxemia on the pharmacokinetics and the electroencephalographic effect of propofol in the rat.

Endotoxemia decreases the dose requirement for anesthetics but no data are available for propofol. A rat model was used in which the influence of endotoxin administration on the pharmacokinetics and pharmacodynamics of propofol was investigated. Chronically instrumented rats were randomly allocated to either a control (n = 9) or an endotoxin (n = 9) group. Six hours after pretreatment with either endotoxin or its solvent, propofol was infused (150 mg x kg(-1) x h(-1)) until isoelectric periods of 5 s or longer were observed in the electroencephalogram. The changes observed in the electroencephalogram were quantified using aperiodic analysis and used as a surrogate measure of hypnosis. The righting reflex served as a clinical measure of hypnosis. The propofol dose needed to reach the electroencephalographic end point in the endotoxin-treated rats was reduced by almost 50% (p < 0.01). This could be attributed to a decrease in propofol clearance and in distribution volume related to the degree of physiologic and metabolic disturbances induced by endotoxin. To investigate changes in end organ sensitivity, the biphasic electroencephalographic effect versus effect-site concentration relationship was studied. This relationship was characterized by descriptors that showed an increased intrinsic efficacy of propofol in the endotoxin group. The effect-site concentration at the return of righting reflex was lower in the endotoxin group. Our study demonstrates that endotoxin-treated animals need a lower dose of propofol to reach the same degree of anesthetic effect which can mainly be attributed to changes in pharmacokinetics.

Animals↗
PubMed1999

Propofol's biphasic effect on GABA(A)-receptor-mediated response of the isolated guinea pig ileum.

This study examines the effect of the anaesthetic agent propofol on the guinea pig ileum and whether this effect derives from an interaction of the drug with GABA receptors. Propofol produced a biphasic effect consisting of a dose-dependent contractile effect (EC(50)=2.2x10(-5)m) followed by an 'after relaxation'. This propofol effect was similar to the one produced by GABA and was bicuculline-sensitive (ID(50)=3.2x10(-7)m). Propofol, at concentrations of 10(-7)and 10(-6)m, potentiated the ileum contractile responses to GABA, but only at the lower dose range of applied GABA, while at a concentration of 10(-5)m, it inhibited the contractile effect over the entire dose range of applied GABA. In addition, while the contractile response of the ileum to exogenously applied acetylcholine was not influenced by propofol at concentrations of up to 7x10(-6)m, it was antagonised by higher concentrations of propofol. In conclusion, the above data permit us to suggest that propofol's contractile effect on the guinea pig ileum is mediated by an interaction of the drug with GABA(A)-receptors.

Acetylcholine↗
PubMed2000

Direct inotropic effects of propofol and adenosine on rat atrial muscle: possible mechanisms.

Experiments were designed to evaluate the mechanisms of propofol and adenosine in rat atrial muscle. Atria were suspended in the isolated organ bath system for isometric tension recording and response to propofol and adenosine were tested in the absence and presence of glibenclamide, N(G)-nitro-arginine-methyl-ester (l-NAME), tetraethylammonium (TEA) and 8-phenyltheophylline (8-PT). The inotropic effect of propofol was elicited by TEA and glibenclamide. In contrast, l-NAME and 8-PT has no effect on the propofol-induced inhibition of atria. Furthermore, atria exhibited a diminished sensitivity to the adenosine-induced negative inotropic effect in the presence of the K(ATP)channel inhibitor glibenclamide, but not the non-specific K(+)channel inhibitor TEA. The adenosine A(1)receptor antagonist 8-PT decreased the responsiveness of adenosine-induced inhibition of atrial muscle. We propose that propofol-induced inotropy is generally mediated by K(+)channels, whereas adenosine-induced inotropy is partially mediated by K(+)channels. Both propofol- and adenosine-induced inotropy were not mediated by nitric oxide release. Our study provides further evidence that there was no contribution of adenosine in the propofol-induced inotropy.

Adenosine↗
PubMed1990

The use of midazolam versus propofol for short-term sedation following coronary artery bypass grafting.

Midazolam and propofol were compared in an open randomized study for postoperative sedation during 12 h of mechanical ventilation in 40 patients following coronary artery bypass grafting. After an intravenous loading dose of midazolam (50 micrograms.kg-1) or propofol (500 micrograms.kg-1), a titrated continuous infusion was administered of midazolam (mean dose 38.1 micrograms.kg-1.h-1 (SEM 2.6)) or propofol (mean dose 909 micrograms.kg-1.h-1 (SEM 100)) together with a narcotic analgesic infusion. During mechanical ventilation midazolam and propofol produced a similar quality of sedation, but recovery (midazolam 66 min (SEM 16); propofol 24 min (SEM 7)) and weaning from the ventilator (midazolam 243 min (SEM 44); propofol 154 min (SEM 33)) where faster with propofol. In the 2 groups administration of an intravenous loading dose caused a significant decrease in mean arterial pressure but hemodynamic tolerance during maintenance infusion was good.

Aged↗
PubMed1990

Comparative evaluation of propofol and thiopentone for total intravenous anaesthesia.

Sixty unpremedicated ASA physical status I or II patients scheduled for surgical procedures of intermediate duration (15 to 60 min) were studied to evaluate the safety and efficacy of propofol, to measure recovery times and to compare the return of psychomotor and cognitive function with thiopentone. Patients were randomly allocated into two groups. Anaesthesia was induced and maintained by either propofol (2.0-2.5 mg.kg-1 followed by a continuous infusion 0.1-0.2 mg.kg-1.min-1) or thiopentone (4.0-5.0 mg.kg-1, and infusion rate 0.16-0.32 mg.kg-1.min-1), titrated to patient response. Succinylcholine was administered to facilitate tracheal intubation and maintain neuromuscular blockade. Induction of anaesthesia was slightly longer with propofol than thiopentone (42.2 vs 29.8 sec) and was smooth with both drugs. Post-intubation increases in heart rate, and systolic and diastolic blood pressures were attenuated by propofol when compared with thiopentone. After the administration of propofol, times to eye opening (6.4 +/- 4.3 vs 13.9 +/- 15.9 min), response to verbal command (7.6 +/- 6.3 vs 15.4 +/- 16.6 min) and orientation (22.7 +/- 12.8 vs 36.2 +/- 23.1 min), were significantly shorter. Psychomotor and cognitive function returned earlier with propofol and fewer side effects were noted. At 24 hr there was no distinguishable difference between groups. Propofol is a safe anaesthetic agent with the potential for early patient discharge and street fitness after outpatient procedures.

Adult↗
PubMed1992

Arterial baroreflex attenuation during and after continuous propofol infusion.

The reduction of arterial blood pressure produced by propofol may be, in part, attributable to impaired baroreflex integrity. The purpose of this study was to investigate arterial baroreflex sensitivity during and after continuous propofol infusion. In urethane anaesthetized rabbits, left renal sympathetic nerves were exposed and placed on a bipolar silver electrode to record renal sympathetic nerve activity (RSNA). Mean arterial pressure (MAP) via a femoral artery and heart rate (HR) by electrocardiogram were continuously recorded. The rabbits were divided into two groups of eight each: Group 1, propofol 5 mg.kg-1 bolus followed by infusion 0.5 mg.kg-1 x min-1; Group 2, propofol 2 mg.kg-1 bolus followed by 0.2 mg.kg-1 x min-1. Phenylephrine pressor and sodium nitroprusside (SNP) depressor tests were carried out before propofol was started (control), at 15 and 30 min during 30 min infusion, and at 15, 30 and 60 min after its discontinuation. The change of RSNA was plotted with respect to every 5 mmHg increment and decrement of MAP to construct sympathetic baroreflex sigmoid curves, and to evaluate baroreflex sensitivity. The baroreflex sensitivity was also evaluated by calculating the ratio of maximum increase of RSNA or HR to SNP-induced maximum decrease of MAP (delta RSNA/delta MAP, delta HR/delta MAP). Despite the same decreases or increases in MAP, RSNA was attenuated after 15 and 30 min of propofol infusion in both groups compared with control (P < 0.05). Decreased delta RSNA/delta MAP gradually returned to the control level 60 min after discontinuation of propofol in Group 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Growth curves of Staphylococcus aureus, Candida albicans, and Moraxella osloensis in propofol and other media.

Propofol, 2,6 diisopropylphenol, in an emulsion formulation (Diprivan), has been associated with postsurgical infections caused by Staphylococcus aureus, Moraxella osloensis and Candida albicans. These organisms were individually inoculated into each of the following media: (1) the emulsion preparation of propofol, (2) Intralipid 10%, (3) pure 2,6 diisopropylphenol, and (4) trypticase soy broth (TSB). The organisms were incubated and subcultured hourly for eight hours at room temperature. Propofol supported the growth of all three organisms, but for S. aureus and M. osloenis, the growth rate was slower in propofol than in TSB (P less than 0.05). There was no difference between the growth rate of any organism in propofol than in Intralipid 10%. The authors conclude that propofol, in the emulsion formulation, supports bacterial growth and, therefore, must be prepared for administration in an aseptic manner. Also, by administering propofol soon after preparation, the risk of introduction of a significant inoculum to the patient will be reduced.

Candida albicans↗
PubMed1994

Intracoronary propofol does not decrease myocardial contractile function in the dog.

The intravenous administration of propofol is associated with a considerable decrease in arterial blood pressure. The present study was undertaken to test the hypothesis that myocardial function is not affected by propofol and therefore does not contribute to the hypotensive effect of this anaesthetic agent. Propofol was administered in anaesthetized, open-chest dogs by direct arterial infusion into the left anterior descending coronary artery (LAD). Mean arterial blood pressure, heart rate, left ventricular pressure, dP/dt, regional lactate and oxygen extraction, as well as coronary blood flow were measured. Diastolic function was determined by calculation of the time constant of isovolumetric relaxation from the left ventricular pressure measurement and dP/dt. Contractility was evaluated by measuring regional systolic shortening in an area of the myocardium supplied by the LAD. This was compared with systolic shortening in the distribution of the circumflex (CIRC) artery and with the effects obtained with the intracoronary administration of thiopentone. Intracoronary infusions of propofol and thiopentone did not produce any change in systemic arterial blood pressure, heart rate, or left ventricular end diastolic pressure. Propofol, at a concentration of 5 or 10 micrograms.ml-1 did not decrease systolic shortening in the area perfused by the LAD while thiopentone (40 micrograms.ml-1) reduced systolic shortening by 33% (P < or = 0.05). Neither drug had an effect on systolic shortening in the CIRC area, LAD blood flow or diastolic function. The results of this study suggest that propofol does not have an effect on myocardial contractility. The hypotension associated with the intravascular administration of propofol is more likely due to either a direct vascular or a central effect.

Animals↗
PubMed1997

Propofol patient-controlled sedation during hip or knee arthroplasty in elderly patients.

PURPOSE: Little information is available regarding the use of patient-controlled sedation (PCS) among the elderly. This study evaluated the safety and efficacy of propofol PCS among elderly patients undergoing hip or knee arthroplasty. METHODS: Forty patients, aged 65-78 yr, undergoing hip or knee arthroplasty under regional anaesthesia were randomized to receive propofol PCS (dose = 0.3 mg.kg-1, delay = three min; n = 20) or anaesthetist-administered midazolam-fentanyl sedation (n = 20). Sedation, anxiety and discomfort visual analogue scores (VAS) were measured, by an independent observer, preoperatively, immediately at the end of surgery and one hour following admission to the postanaesthetic care unit (PACU). Cognition was evaluated, using an abbreviated Mini Mental Status Examination, preoperatively and in the PACU. Patient satisfaction, based on VAS and a brief questionnaire, was measured in the PACU. The incidence of intraoperative complications was also compared. RESULTS: Patient satisfaction was high in each group. Sedation and anxiety VAS were similar in each group. A high incidence of pain with drug injection was noted among patients receiving propofol (80%). Transient deeper levels of sedation (6 vs 1; P = 0.05) were observed more commonly in the propofol PCS group. CONCLUSION: Propofol PCS provides effective sedation. Using a propofol dose of 0.3 mg.kg-1, transient episodes of deeper sedation were noted more frequently among patients receiving PCS. These episodes did not require intervention but, suggest that this propofol PCS dose approaches the limit of safety and should be further reduced for some elderly patients.

Adjuvants, Anesthesia↗
PubMed1994

Adjuvant propofol enables better control of nausea and emesis secondary to chemotherapy for breast cancer.

We investigated the prophylactic antiemetic effect of added low-dose infusion of propofol in patients exhibiting nausea and vomiting refractory to dexamethasone and serotonin antagonist during non-cisplatin chemotherapy for breast cancer. In a prospective open longitudinal study, 117 patients who had more than five episodes of nausea and vomiting in their first chemotherapy cycle during the first 24 hr completed the study. They received in addition to the usual prophylactic antiemetic regimen a continuous intravenous infusion of 1 mg.kg-1.hr-1 propofol started four hours before chemotherapy and continued up to 24 hr for the two subsequent cycles. The number of vomiting/nausea episodes, level of sedation, patient activity, appetite and preference for future chemotherapy cycles were assessed. In the propofol supplemented cycles 90 and 80% of patients, during the 1st and 2nd propofol-assisted cycle respectively, were free of nausea and vomiting during the first 24 hr after chemotherapy. Patients were more frequently active and had more appetite during the propofol-assisted cycles. No propofol-associated side effects were observed. We conclude that the addition of a subhypnotic infusion of propofol enables better control of nausea and vomiting caused by non-cisplatin chemotherapy in the first 24 hr post-treatment.

Aged↗
PubMed2002

Sevoflurane and isoflurane, but not propofol, decrease mivacurium requirements over time.

PURPOSE: Volatile anesthetic agents potentiate neuromuscular blockade, but the magnitude of potentiation appears to be time dependent. The time course of this interaction was studied by measuring mivacurium infusion rates during sevoflurane, isoflurane and propofol anesthesia. METHODS: After informed consent, anesthesia was induced in 48 ASA physical status I-II adults with propofol, fentanyl and mivacurium 0.25 mg.kg(-1) and maintained with N(2)O (60%) and one of the three agents chosen at random: sevoflurane 1.9%; isoflurane 1.2%; or propofol 100-150 microgram.kg(-1).min(-1). Train-of-four stimulation was applied every 15 sec to the ulnar nerve. Neuromuscular blockade was monitored with accelerometry. At 5% recovery of the first twitch (T1), a mivacurium infusion was started and adjusted every five minutes to maintain 90-95% T1 depression. RESULTS: The time to 5% T1 recovery after the initial dose was similar in all groups (13-15 min). Fifteen minutes after the start of the infusion mivacurium requirements were greater (P < 0.05) in the propofol group (7.5 +/- 1.7 microgram.kg(-1).min(-1); mean +/- SD) than in either isoflurane (4.7 +/- 1.6 microgram.kg(-1).min(-1)) or sevoflurane (4.5 +/- 1.5 microgram.kg(-1).min(-1)) group. Then, the rate remained stable for propofol (6.2 +/- 1.4 microgram.kg(-1).min(-1) after 90 min of infusion) while it decreased with isoflurane to 2.9 +/- 1.6 microgram.kg(-1).min(-1) at 90 min (P < 0.05 vs propofol) and to 1.4 +/- 1.0 microgram.kg(-1).min(-1) in the sevoflurane group (P < 0.05 vs propofol and isoflurane). CONCLUSION: Sevoflurane and isoflurane do not prolong the effect of a bolus dose of mivacurium, but potentiation increases with time from 30-105 min of exposure. This interaction is greater with sevoflurane than isoflurane.

Adult↗
PubMed2002

Rocuronium pharmacokinetic-pharmacodynamic relationship under stable propofol or isoflurane anesthesia.

PURPOSE: To compare the pharmacokinetics, pharmacodynamics and the concentration-effect relationship of rocuronium in patients under stable propofol or isoflurane anesthesia. METHODS: Ten patients were randomized to receive fentanyl, propofol and nitrous oxide (60%) or fentanyl, thiopental, isoflurane (1.2% end-tidal concentration) and nitrous oxide (60%). To obtain good intubation conditions and maintain adequate muscle relaxation during surgery, patients received two bolus doses of rocuronium: 0.5 mg x kg(-1) (1.7 x ED95) at induction followed one hour later by 0.3 mg x kg(-1) (1 x ED95). Arterial blood samples were obtained over six hours after the second bolus dose. Plasma concentrations of rocuronium were measured using high pressure liquid chromatography. Muscle twitch tension was monitored by mechanomyography for the two doses. Pharmacokinetic and pharmacodynamic parameters were determined. RESULTS: No differences in rocuronium pharmacokinetic parameters were observed between both groups. After the second bolus, clinical duration was 20 +/- 6 min in the propofol group vs 39 +/- 8 min in the isoflurane group (P <0.05). The effect compartment concentration corresponding to 50% block, EC50, was higher under propofol anesthesia: 1008 vs 592 microg x L(-1) (P <0.05). CONCLUSION: Rocuronium body disposition is similar under stable propofol or isoflurane anesthesia. In contrast to isoflurane, propofol does not prolong the neuromuscular block. Therefore, the potentiating effect of isoflurane is of pharmacodynamic origin only, as explained by an increased sensitivity at the neuromuscular junction. In contrast with isoflurane anesthesia where the dose of rocuronium has to be decreased under stable conditions, no dose adjustment is required under propofol anesthesia.

Adult↗
PubMed2004

Sevoflurane for interventional neuroradiology procedures is associated with more rapid early recovery than propofol.

PURPOSE: Sevoflurane and propofol are both suitable for neuroanesthesia but have not previously been compared as maintenance agents for long duration (one to five hours) procedures. METHODS: Using a multicentre international study protocol, 103 patients were randomized to receive either sevoflurane or propofol for maintenance of anesthesia during interventional neuroradiology procedures. After a standardized induction of anesthesia with propofol, 53 patients received sevoflurane 1 to 3% with 60% nitrous oxide (N(2)O) in oxygen (O(2)), and 50 patients received propofol 4 to 10 mg x kg(-1) x hr(-1) with 60% N(2)O in O(2). Maintenance agents were titrated against systemic arterial blood pressure (baseline mean arterial pressure +/- 20%). Recovery times, changes in sedation, pain, nausea and vomiting and psychomotor function during recovery and use of rescue medication were recorded. RESULTS: The group receiving sevoflurane had a more rapid recovery to spontaneous ventilation, extubation, eye opening and orientation compared to the group receiving propofol (3 vs 4 min, P = 0.01; 5 vs 6 min, P = 0.015; 7 vs 10 min, P < 0.001; 13 vs 17 min, P = 0.028; respectively). Sedation, pain, nausea and vomiting, and psychomotor function scores were similar in the two groups. Use of opioid boluses and vasopressors were similar. CONCLUSION: The use of sevoflurane for maintenance of anesthesia for prolonged neuroradiological procedures is associated with more rapid early recovery than propofol and is associated with similar side effects. Sevoflurane and propofol can both be recommended for these procedures. The clinical benefit of the more rapid recovery with sevoflurane is unknown.

Adolescent↗
PubMed2004

Desflurane increases cerebral blood flow velocity when used for rapid emergence from propofol anesthesia in children.

PURPOSE: Desflurane may be used to replace propofol at the end of anesthesia to facilitate rapid emergence. This study determined the effect of administering desflurane during emergence of anesthesia on middle cerebral artery blood flow velocity (Vmca) in children anesthetized with propofol. METHODS: Thirty healthy children aged one to six years scheduled for orchidopexy or hypospadias repair under general anesthesia were enrolled. Anesthesia was maintained with a propofol infusion targeting an estimated serum level of 3 microg x mL(-1), remifentanil 0.2 microg x kg(-1) x min(-1) and a caudal epidural block. Transcranial Doppler sonography was used to measure Vmca at five-minute intervals. In half the patients, propofol was substituted with desflurane 1 MAC, 30 min prior to the end of the surgical procedure. Once steady-state had been achieved recordings of Vmca, heart rate, and mean arterial pressure were resumed. Upon termination of the surgical procedure, the maintenance agent was discontinued and recordings continued at one-minute intervals during emergence of anesthesia. RESULTS: There were no demographic differences between the two groups. Vmca increased from 37.2 +/- 3.1 cm x sec(-1) to 57.7 +/- 4.1 cm x sec(-1) when propofol was changed to desflurane (P < 0.01). Upon emergence of anesthesia, Vmca decreased from 57.8 +/- 4.2 cm x sec(-1) to 37.8 +/- 3.2 cm x sec(-1) in the desflurane group (P < 0.01) but remained unchanged in the propofol group. CONCLUSION: Desflurane is associated with an increase in cerebral blood flow velocity when used to facilitate rapid emergence following a propofol infusion in children. This may be of clinical significance in patients with intracranial pathology.

Anesthesia Recovery Period↗
PubMed2000

Autonomic circulatory and cerebrocortical responses during increasing depth of propofol sedation/hypnosis in humans.

PURPOSE: To describe the relative effects of graded central nervous system (CNS) depression, using increasing propofol infusion rates, on neurovegetative brainstem-mediated circulatory control mechanisms and higher cortical activity in healthy humans. METHODS: Propofol was administered using an infusion scheme designed to achieve three target blood concentrations in ten healthy volunteers. Blood propofol concentrations and sedation scores were determined at baseline, during the three propofol infusion levels, and 30 min into the recovery period. Electroencephalographic (EEG) power was measured in three frequency bands to quantify cortical activity, and autonomic heart rate control was quantified using spontaneous baroreflex assessment and power spectral analysis of pulse interval. RESULTS: Sedation scores closely paralleled propofol blood concentrations (0, 0.53 +/- 0.34, 1.24 +/- 0.21, 3.11 +/- 0.80, and 0.96 +/- 0.42 microg x mL(-1) at baseline, three infusion levels and recovery respectively), and all subjects were unconscious at the deepest level. Indices of autonomic heart rate control were decreased only at the deepest levels of CNS depression, while EEG effects were apparent at all propofol infusion rates. These EEG effects were frequency specific, with power in the beta band being affected at light levels of sedation, and alpha and delta power altered at deeper levels. CONCLUSIONS: The results of this study support a relative preservation of neurovegetative circulatory control mechanisms during the early stages of CNS depression using gradually increasing rates of infusion of propofol. Indices of circulatory control did not reliably reflect depth of sedation.

Adult↗