Total intravenous anaesthesia with propofol or etomidate

In combination with fentanyl, propofol was compared with etomidate for total intravenous anaesthesia in 21 women (ASA Grades I-II) admitted for elective hysterectomy. They received either propofol (bolus 1.5 mg kg-1, infusion 9 mg kg-1 h-1 for 10 min thereafter 6 mg kg-1 h-1) or etomidate (bolus 0.10 mg kg-1, infusion 3 mg kg-1 h-1 reduced to 0.6 mg kg-1 h-1). Fentanyl 10 micrograms kg-1 was given for induction followed by an infusion of 30 micrograms kg-1 h-1 for 10 min reduced to 6 micrograms kg-1 h-1 for the first hour and successively reduced over time. Induction was smooth and maintenance easy to manage in both groups. There was no difference in time from end of infusion until extubation, but the time until the patients could report their date of birth was significantly shorter in the propofol group. Nausea and vomiting were more pronounced in the etomidate group, and mental side-effects were only seen after etomidate. After 3 months, more patients in the etomidate group complained of reduced power of concentration. We conclude that total intravenous anaesthesia with either propofol or etomidate is equally easy to manage, but in the recovery situation propofol was advantageous in time and quality.     

Cerebrospinal fluid concentrations of propofol during anaesthesia in humans

The concentration of propofol in and surrounding the human brain during propofol anaesthesia is unknown. We measured simultaneously the concentration of propofol in cerebrospinal fluid (CSF) from an indwelling intraventricular catheter and the concentration in arterial blood in five neurosurgical patients before, during induction (at 2.5 and 5 min) and during a maintenance propofol infusion (at 15 and 30 min). After induction of anaesthesia with propofol 2 mg kg-1, anaesthesia was maintained with an infusion of 8 mg kg-1 h-1 for 15 min and then reduced to 6 mg kg-1 h-1. The plasma concentration of propofol increased rapidly during induction and reached a plateau concentration of mean 2.24 (SD 0.66) micrograms ml-1 after 5 min. The concentration of propofol in CSF showed a slower increase during induction and remained almost constant at 35.5 (19.6) ng ml-1 at 15-30 min after induction. The CSF concentration of propofol that we measured was 1.6% of the plasma concentration and consistent with the high protein binding of the drug in plasma.      

Recovery after anesthesia with propofol in otorhinolaryngologic surgery of brief duration

This study was designed to assess recovery from total intravenous anaesthesia with propofol for short ENT procedures. Twenty-six patients (ASA I and II) were assigned to two groups of thirteen: one breathed air (Laser laryngeal microsurgery), the second N2O-O2 (FIO2 : 0.5) (various ENT procedures). The induction sequence was exactly the same for both groups: oral premedication with 10 mg diazepam one hour before surgery, I mg pancuronium bromide, 2 micrograms X kg-1 fentanyl, denitrogenation within 3 min, after which propofol was delivered (2.5 mg X kg-1). When the eye-lash reflex had disappeared (time recorded), 1.5 mg X kg-1 suxamethonium was given and laryngotracheal intubation carried out. A continuous infusion of propofol (9 mg X kg-1 X h-1) was started. Surgery began 5 +/- 2 min after the start of propofol infusion. The durations of anaesthesia, surgery and propofol infusion were similar in both groups. To have good surgical conditions, it was necessary to give repeated doses of propofol for 15 patients. Thus, the total dose of propofol was significatively different between the two groups: 24.5 +/- 6.7 mg X kg-1 X h-1 in group "air" versus 16 +/- 3.6 mg X kg-1 X h-1 in group "N2O-O2" (p less than 0.001). Extubation occurred within 16 +/- 8 min in group "air", being more rapid in group "N2O-O2" (11 +/- 9 min; no significant difference). Recovery was assessed with two psychomotor tests: choice reaction time (CRT) and tracing test (TT).(ABSTRACT TRUNCATED AT 250 WORDS)     

A comparison of bispectral index and ARX-derived auditory evoked potential index in measuring the clinical interaction between ketamine and propofol anaesthesia

We evaluated the effects of a bolus (0.4 mg.kg-1) and continuous infusion (1 mg.kg-1.h-1) of ketamine on Bispectral Index (BIS) and A-Line(R) ARX Index (AAI) during propofol anaesthesia. We included 15 ASA I patients scheduled for general anaesthesia. Induction was performed by infusion of propofol at 100 ml.h-1 until loss of consciousness. Both BIS and AAI monitors responded appropriately at that time. The calculated effect site concentration of propofol at loss of consciousness was maintained by means of a computer controlled infusion system. A 'pseudo' steady-state effect site concentration was reached after 4 min. After 1 min of baseline measurements, ketamine was administered. BIS values increased from the 3rd to the 8th min after the administration of ketamine. The AAI showed no significant increase or decrease, but between-patient variability increased.     

Recovery characteristics using isoflurane or propofol for maintenance of anaesthesia: a double-blind controlled trial

We studied 114 female patients (ASA 1 or 2) who were within 20% of ideal body weight and who were scheduled to undergo gynaecological laparoscopy which required supplementation with an opioid (groups IA and PA), or dental procedures which did not require opioid supplementation (groups IO and PO). A computerised package of psychomotor tests was performed before surgery. Anaesthesia was induced with propofol 2.5 mg.kg-1 and all patients received atracurium 0.3 mg.kg-1 and 67% nitrous oxide in oxygen. Patients in group IA received isoflurane 1% (inspired), and alfentanil 10 micrograms.kg-1 as a bolus and 10 micrograms.kg-1.h-1 as an infusion. Patients in group PA received propofol 9 mg.kg-1.h-1 as an infusion, decreasing to 6 mg.kg-1.h-1 after 15 min, together with alfentanil 10 micrograms.kg-1.h-1. Patients in groups IO and PO received isoflurane and propofol in the regimens described for groups IA and PA, but without alfentanil. Recovery was assessed by a blinded observer who recorded times to awakening (eye opening) and orientation (giving date of birth), and who repeated the psychomotor tests at 1, 3 and 5 h. Linear analogue scales of mood, nausea and pain were obtained and other side effects were noted in the succeeding 48 h. A matched control group of 25 females (who were not anaesthetised) underwent psychomotor testing on four occasions in order to assess the 'learning effect' of repeated recovery testing. The analysis of recovery tests did not assume a normal distribution.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative effects of thiopentone and propofol on respiratory resistance after tracheal intubation

To compare the effects of propofol and thiopentone on tracheal intubation-induced bronchoconstriction, 37 patients were allocated randomly to anaesthesia with either thiopentone 4 mg kg-1 followed by a 15-mg kg-1 h-1 continuous infusion or propofol 3 mg kg-1 followed by a 9-mg kg-1 h-1 continuous infusion. Intubation was facilitated by vecuronium 0.1-0.2 mg kg-1. Respiratory system resistance (Rrs) was measured by a CP-100 pulmonary function monitor, 5 min after intubation. The 5-min post-intubation Rrs values were significantly lower in the propofol group (8.5 (SD 1.5) cm H2O litre-1 S-1) than in the thiopentone group (10.9 (3.2) cm H2O litre-1 S-1). Thirty minutes after commencing isoflurane-nitrous oxide anaesthesia, Rrs declined by 17.5 (SEM 3.6)% from baseline in the thiopentone group, but by only 1.6 (2.6)% in the propofol group. We conclude that the dose of propofol administered provided more protection against tracheal intubation- induced bronchoconstriction than an induction dose of thiopentone.      

Comparison of propofol and propanidid administered at a constant rate

So as to compare the anaesthesia obtained using propofol with that obtained using propanidid, 40 ASA I patients, aged between 18 and 50 years, who were to undergo elective orthopaedic or plastic surgery lasting more than 60 min, were randomly divided into two equal groups, one receiving propofol (PF) and the other propanidid (PD). All the patients received 0.5 mg atropine, 100 mg pethidine and 7.5 mg droperidol (10 mg if weight greater than 60 kg) intramuscularly 45 min before induction. Patients in group PF were then given 2 mg.kg-1 propofol over 1 min and 0.9 microgram.kg-1 fentanyl over 3 min, followed by a constant rate infusion of 5 mg.kg-1.h-1 propofol and 3 micrograms.kg-1.h-1 fentanyl. For PD patients, the doses of fentanyl were identical; they were given 10.6 mg.kg-1 propanidid over 3 min for induction, and 37 mg.kg-1.h-1 for maintenance. All the patients were intubated and ventilated mechanically. The usual anaesthetic parameters were monitored at induction, during surgery, and during recovery. Consciousness was lost more quickly with propofol (p less than 0.05), but the corneal reflex returned more rapidly in group PD (p less than 0.02). The time required for a full return to normal consciousness was identical in both groups. The fall, during induction, and the increase, during recovery, of Pasys were greater in group PD (p less than 0.05 and less than 0.001 respectively). Padia and heart rate were lower in group PF after the 30th min (p less than 0.05 and less than 0.01 respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of pre-induction glycopyrronium on the haemodynamic response of elderly patients to anaesthesia with propofol

This study investigated whether pretreatment with glycopyrronium can attenuate the hypotension caused by anaesthesia of the elderly with propofol. Twenty elderly patients (77.1 +/- 2.44 years, mean +/- SEM) of ASA physical status 2 or 3 scheduled for elective urological procedures were given glycopyrronium 0 (n = 10) or 5 micrograms.kg-1 (n = 10) in a randomised, double-blind manner, 5 min before induction of anaesthesia with propofol infused at 600 ml.h-1 (average induction dose 1.7 +/- 0.06 mg.kg-1, mean +/- SEM) followed by maintenance with a propofol infusion at 10 mg.kg-1.h-1. Although glycopyrronium significantly increased heart rate (p less than 0.01, ANOVA), the decrease in blood pressure 2 and 5 min after induction was similar in both groups. The study had a power of 80% to detect a 20 mmHg difference in systolic arterial pressure between treatment groups with p less than 0.05.     

Recovery and discharge of patients after long propofol infusion vs isoflurane anaesthesia for ambulatory surgery

Fifty unpremedicated patients scheduled for outpatient restorative dentistry and/or oral surgery lasting 2 to 4 h were anaesthetized with either propofol infusion or isoflurane inhalation. Before induction of anaesthesia with propofol (2.5 mg.kg-1), all patients were given 75 mg of diclofenac and 0.01 mg.kg-1 vecuronium intravenously. Intubation was facilitated with suxamethonium (1.5 mg.kg-1) and anaesthesia was maintained in random order either with propofol infusion (12 mg.kg-1.h-1 for the first 20 min, 9 mg.kg-1.h-1 for the next 20 min, and 6 mg.kg-1.h-1 for the rest of the anaesthesia) or with isoflurane (inspired concentration 1-2.5%), both with nitrous oxide and oxygen (30%). The patients breathed spontaneously using a non-rebreathing circuit. Patients given propofol infusion became re-orientated faster (11.0 +/- 5.5 min vs. 16.5 +/- 7.5 min; P less than 0.01) and at 30 min walked along a straight line better (P less than 0.01). At 60 min, none of the propofol patients displayed an unsteady gait, whereas 11 of the 25 isoflurane patients did (P less than 0.001). None of the patients receiving propofol had emesis at the clinic, compared with 10 of the 25 patients receiving isoflurane (P less than 0.001). The overall incidence of emesis was 2 of 25 and 14 of 25 in the propofol and isoflurane groups, respectively (P less than 0.01). Patients receiving propofol were discharged home earlier than patients receiving isoflurane (80 +/- 14 min and 102 +/- 32 min, respectively; P less than 0.01). It is concluded that propofol allows early discharge of patients, even after long anaesthesias.     

Propofol auto-co-induction as an alternative to midazolam co-induction for ambulatory surgery

We propose the use of an intravenous propofol/propofol auto-co-induction technique as an alternative to propofol/midazolam for induction of anaesthesia. We have studied 54 unpremedicated ASA 1 or 2 patients undergoing day-stay anaesthesia for minor orthopaedic surgery. All received 10 micrograms.kg-1 or alfentanil before induction, followed by either midazolam 0.05 mg.kg-1, propofol 0.4 mg.kg-1 or saline, and 2 min later, a propofol infusion at a rate of 50 mg.kg-1.h-1 until loss of eyelash reflex. We compared pre- and postinduction haemodynamic changes, complications at insertion of a laryngeal mask airway and recovery from anaesthesia in the three groups. Both co-induction techniques showed less postinduction hypotension and significant reduction of the total induction dose of propofol when compared to the control group. In the propofol/propofol group there was a decreased incidence of apnoea during induction of anaesthesia. These patients were discharged from hospital 2 h after the end of anaesthesia whereas patients in the midazolam/propofol group were discharged after 2 1/2 h (p < 0.001).     

Effects of graded infusion rates of propofol on cardiovascular haemodynamics, coronary circulation and myocardial metabolism in dogs

We have studied the effects of a 30-min infusion of propofol 6, 9, 12, 15, 18 and 21 mg kg-1 h-1 on cardiovascular haemodynamics, coronary circulation and myocardial metabolism in 12 mongrel dogs. Mean plasma concentrations of propofol after infusion of 6 and 21 mg kg-1 h-1 increased from 2.9 (SEM 0.3) to 11.5 (0.1) micrograms ml-1. Propofol produced a progressive decrease in arterial pressure. Heart rate tended to decrease at 15, 18 and 21 mg kg-1 h-1 and cardiac index decreased significantly at infusion rates > or = 9 mg kg-1 h-1. Systemic vascular resistance tended to increase except at 21 mg kg-1 h-1 and left ventricular systolic and diastolic function were depressed. Both coronary sinus blood flow and myocardial oxygen consumption decreased in parallel with a decrease in left ventricular minute work index without producing lactate. Propofol produced progressive decreases in coronary blood flow and myocardial oxygen consumption but did not exert adverse effects on the coronary circulation.      

Relaxant effect of propofol on the airway in dogs

Propofol has been suggested to produce airway relaxant effects in vivo, although the mechanism is unclear. We have evaluated the bronchodilating effect of propofol using a direct visualization method with a superfine fibreoptic bronchoscope. We studied 21 mongrel dogs anaesthetized with pentobarbital 30 mg kg-1 i.v. and pancuronium 0.2 mg kg-1 h-1. The animals were allocated randomly to one of three groups (n = 7 in each): propofol group, atropine-propofol group and histamine- propofol group. The trachea was intubated using a tracheal tube that had a second lumen for insertion of the bronchoscope to monitor continuously bronchial cross-sectional area (BCA). BCA was measured using the NIH Image program. In the propofol group, dogs were given the following doses of propofol at 10-min intervals: 0 (saline), 0.2, 2.0 and 20 mg kg-1 i.v. In the atropine-propofol group, saline, atropine 0.2 mg kg-1 and propofol 20 mg kg-1 were given at 10-min intervals. In the histamine-propofol group, bronchoconstriction was elicited with histamine 10 micrograms kg-1 and 500 micrograms kg-1 h-1 until the end of the experiment. Thirty minutes after the start of infusion of histamine, propofol (0, 0.2, 2.0 and 20 mg kg-1) was administered. Changes in BCA were expressed as percentage of basal area. Histamine decreased BCA by 39.2 (SEM 5.4%). Propofol increased significantly basal and histamine-decreased BCA in a dose-dependent manner by 18.4 (4.5%) and 15.8 (4.9%), respectively after 20 mg kg-1 i.v. However, propofol following atropine i.v. did not increase BCA (129.9 (8.2)% after atropine vs 125.7 (8.9)% after propofol). Therefore, the relaxant effect of propofol may be a result of reduction in vagal tone.      

Ventilatory effects of a propofol infusion using a method to rapidly achieve steady-state equilibrium

The ventilatory effects of a propofol infusion were studied in 10 females premedicated with atropine and nine with papaveretum and atropine. The infusion, at a rate of 20 mg kg-1 h-1 for 5 min, reducing to 12 mg kg-1 h-1 for 10 min and then 6 mg kg-1 h-1 thereafter, was known to produce a steady-state plasma propofol concentration for 20-25 min after 25 min from commencement. Minute ventilation, tidal volume, frequency and response to breathing carbon dioxide were measured before the infusion and during the steady-state period. Propofol decreased minute ventilation to 56% and 46% (P less than 0.01) of their mean control values in the atropine and papaveretum groups, respectively. Mean tidal volume was decreased to 41-44% (P less than 0.02) by propofol, but a tachypnoea observed in the atropine group during the infusion was absent in the papaveretum group. Propofol alone had no effect on the slopes of the carbon dioxide response curves but did produce a shift to the right (P less than 0.05). Following papaveretum premedication the minute ventilation-carbon dioxide response curve slope, was decreased to 55% of its mean control volume value by the infusion, but this failed to reach statistical significance.     

Maintenance of anaesthesia with propofol--a comparative study of a stepdown infusion of propofol and a low dose infusion supplemented by incremental doses.

Forty-four patients, ASA Grade I or II, had anaesthesia induced with propofol at 100 mg min-1 followed by a maintenance rate of 6 mg kg-1 h-1 or a stepdown regimen of 10 mg kg-1 h-1 for 10 min, 8 mg kg-1 h-1 for the next 10 min and at 6 mg kg-1 h-1 thereafter. Anaesthesia was maintained with propofol infused using an Ohmeda 9000 pump supplemented by nitrous oxide and oxygen (2:1) in a Bain circuit with spontaneous ventilation. Incremental doses of 20 mg of propofol were given to both groups as clinically indicated to maintain anaesthesia. Both methods provided satisfactory maintenance of anaesthesia but significantly more incremental doses were required in the group receiving the steady rate infusion. However, a lower cumulative dose was required up to 30 min in this group but not by 40 min. A comparable fall in systolic and diastolic blood pressure and heart rate was seen in both groups. There was no difference in the recovery times between the groups and the total dose did not correlate with time to recovery.     

右美托咪啶与丙泊酚用于小儿心导管术麻醉维持的比较

目的 右美托咪啶(dexmedetomidine,DEX)为α2肾上腺素受体激动剂,目前较多研究正在探索其用于小儿麻醉的可行性.研究比较了DEX与丙泊酚用于小儿心导管术的维持麻醉的药效学.方法 选择40例ASA Ⅱ～Ⅲ级、22月～67月、体重11 kg～28 kg导管介入治疗患儿,进入导管室后静注氯胺酮2 mg/kg,...     

Use of a continuous infusion of propofol in maintaining anesthesia

This open, non comparative study was designed to establish a suitable dose regime for propofol when used as the main anaesthetic agent and given as a continuous infusion. Thirty patients (ASA I and II) were studied; five received muscle relaxants and were excluded from the analysis of maintenance and recovery. Immediately after an i.v. bolus dose of fentanyl (2 micrograms X kg-1), anaesthesia was induced in all patients with a mean dose of 2.03 mg X kg-1 propofol. Apnoea at induction was seen in 14 patients, with a mean duration of 151 s (range: 20 to 360 s). Mean, systolic and diastolic arterial pressures and heart rate decreased slightly but statistically significantly following induction. Fourteen patients, four of whom received propofol into a vein of the hand, noted pain on the injection site without venous sequelae immediately nor 24 h after anaesthesia. The mean duration of anaesthesia from induction to the patient ability to obey a simple command was approximately 40 min (range: 10 to 95 min). The mean infusion rate of propofol during maintenance was 0.86 +/- 0.04 mg X kg-1 X min-1. During maintenance, a satisfactory depth of anaesthesia was achieved in 23 patients without any further bolus injection of propofol. The mean time from stopping the infusion to eye opening on verbal command was 6.2 min, whilst that for orientation was 8.4 min. The anaesthesist assessed the quality of recovery as good or adequate in all the patients, who all were satisfied by the anaesthesia. No major adverse reactions occurred during or after anaesthesia and the incidence of minor side-effects was low.     

Propofol versus etomidate in short-time urologic surgery]

Thirty patients, scheduled for short urological surgical procedures and ranked ASA 1 or 2, were randomly assigned to two homogenous groups. In group P, they were given a 2 mg.kg-1 bolus of propofol and 10 micrograms.kg-1 of alfentanil, followed by a continuous infusion of propofol (5 mg.kg-1.h-1) and 5 micrograms.kg-1 doses of alfentanil. In group E, they were given a 0.3 mg.kg-1 bolus of etomidate, followed by an infusion (1.5 mg.kg-1.h-1). The doses of alfentanil were the same as in group P. Further doses of either propofol (0.5 mg.kg-1) or etomidate (0.2 mg.kg-1) were used should anaesthesia prove not to be deep enough. The patients were not intubated, and breathed spontaneously. Surgery lasted a mean of 18.3 +/- 11.8 min (group P) and 18.8 +/- 9.4 min (group E). The following parameters were studied: the amount of each agent required for maintenance of anaesthesia, the duration of apnoea at induction, the quality of anaesthesia and of muscle relaxation, adverse effects (coughing, trismus, restlessness, nausea, vomiting), the time required for recovery, and its quality. In group P, there was a 27% decrease in arterial pressure, without any tachycardia or hypoxia, together with a quick recovery of excellent quality. On the other hand, in group E, there was little or no haemodynamic alteration, but there often was a trismus at induction. Hypoxia also occurred during induction with etomidate, being severe enough in one case to require tracheal intubation and artificial ventilation. The reasons for this hypoxia seemed to be the apnoea and the trismus, which tends to hinder assisted ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Propofol anaesthesia and metabolic acidosis in children

BACKGROUND: We aimed to investigate the effect of propofol infusion anaesthesia on acid-base status and liver and myocardial enzyme levels of children during short-term anaesthesia. METHODS: Thirty-six children, aged 3-12 years, were randomized into two groups. In group P (n = 18), induction and maintenance were performed with propofol, 3 mg x kg-1 and 20, 15 and 10 mg x kg-1 x h-1, respectively. In group H (n = 18) following induction with 5 mg x kg-1 thiopenthal, anaesthesia was maintained with 2-3% halothane. Blood samples were obtained following anaesthesia induction and 30, 60 and 120 min after discontinuation of anaesthesia. RESULTS: There was no difference in lactate dehydrogenase, myocardial creatininephosphokinase, aspartate aminotransferase, alanine aminotransferase and cholesterol levels between and within the groups. All postoperative triglyceride levels were higher and pH levels were lower in group P than group H (P < 0.05) and there was no difference within the groups. CONCLUSIONS: In these healthy patients, short-term use of propofol did not result in significant acidaemia, nor alterations in hepatic or myocardial enzyme levels.     

Cardiopulmonary bypass-induced changes in plasma concentrations of propofol and in auditory evoked potentials

Unbound, rather than total, plasma concentrations may be related to the anaesthetic action of propofol. Therefore, we measured plasma concentrations of propofol and recorded Nb wave latencies of auditory evoked potentials (AEP) during continuous infusion of propofol in 15 patients undergoing coronary artery bypass grafting (CABG) surgery. After induction of anaesthesia with fentanyl, propofol was infused continuously at a rate of 10 mg kg-1 h-1 for 20 min, and then the rate was reduced to 3 mg kg-1 h-1. Administration of heparin before cardiopulmonary bypass (CPB) did not affect total or unbound propofol concentration. Initiation of CPB decreased mean total propofol concentration from 2.6 to 1.7 micrograms ml-1 (P < 0.01). Simultaneously, mean unbound propofol concentration remained at 0.06 micrograms ml-1 because of a slight increase in the mean free fraction of plasma propofol (from 2.3 to 3.5%; P > 0.05). During hypothermic CPB, mean total propofol concentration increased to concentrations measured before bypass (to 2.1 micrograms ml-1; P > 0.05 vs value before CPB) and the mean unbound propofol concentration was at its highest (0.07 microgram ml-1; P < 0.05 vs value before heparin). After CPB and administration of protamine, the mean total propofol concentration remained lowered (1.7 micrograms ml-1; P < 0.05 vs value before heparin) and the mean unbound propofol concentration returned to the level measured before heparin (P < 0.001 vs value during hypothermia). The latency of the Nb wave from recordings of AEP increased after induction of anaesthesia, reached its maximum during hypothermia and was prolonged during the subsequent phases of the study. The latency of the Nb wave did not correlate with total or unbound propofol concentration. We conclude that the changes in total and unbound concentrations of plasma propofol were not parallel in patients undergoing CABG. During CPB or at any other time during the CABG procedure, the unbound propofol concentration did not decrease and Nb wave latency was prolonged compared with baseline values measured after induction of anaesthesia before the start of CPB.      

Comparison of propofol and methohexital for dental and maxillofacial surgery

A prospective study has been undertaken to compare a new intravenous anaesthetic agent, propofol, to methohexitone in 40 ASA I or II patients aged between 18 and 50 years undergoing maxillo-facial surgery and divided into two groups. Intramuscular premedication was standardized for all patients. In group I, propofol 2 mg X kg-1 was injected over 1 min in a peripheral venous line with fentanyl 0.86 microgram X kg-1, followed by an infusion of propofol 5 mg X kg-1 X h-1 and fentanyl 3 micrograms X kg-1 X h-1. In group II, the fentanyl dosage was the same as in group I, whilst methohexitone 3 mg X kg-1 was given for induction and 4.5 mg X kg-1 X h-1 for maintenance of anaesthesia. The following were recorded during induction, maintenance and recovery; haemodynamic parameters using a non invasive method; respiratory parameters; quality of anaesthesia; side-effects. Statistical analysis was performed using the Student t test and qualitative analysis using the Schwartz comparison test at 2%. The following results were found: the quality of anaesthesia with propofol was superior to that of methohexitone during the three stages of anaesthesia. The duration of induction was similar in both groups, but the quality of induction (occurrence of more minor side-effects; p less than 0.05) and intubation was in favour of propofol (p less than 0.05). During maintenance, stability of anaesthesia and a lesser incidence of side-effects were again in favour of the propofol group, in which a slower rate was also found (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)