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PubMed2001

Being awake intermittently during propofol-induced hypnosis: a study of BIS, explicit and implicit memory.

BACKGROUND: Being awake during anaesthesia is a serious complication. An anaesthetic depth monitor must discriminate in real time between wakefulness and unconsciousness. The present study created a period of wakefulness during propofol-induced hypnosis. Bispectral index (BIS), explicit and implicit memories of the awake period were investigated. METHODS: Ten volunteers were studied. The calculated brain concentration of a target controlled infusion of propofol was increased until loss of response (LOR) to verbal command and then propofol was stopped. When fully awake, volunteers were presented with a picture, sound and smell. Propofol infusion was restarted until LOR and then ceased. BIS and the calculated brain concentration of propofol were recorded every minute. A structured interview was conducted for explicit memories after awakening and for explicit as well as implicit memories the day after. RESULTS: Median BIS-index for the transition between awake and asleep and vice versa differed significantly. It was not possible, however, to establish any threshold value or zone for discriminating between wakefulness and LOR due to the large inter-individual variations in BIS-index. No volunteer could explicitly recall any of the stimuli presented during the period of wakefulness. CONCLUSION: The BIS-index decreases with increasing sedation but because of the large individual variations, the real-time BIS-index for the individual subject cannot reliably discriminate wakefulness from unconsciousness during propofol infusion. Propofol causes such profound amnesia that lack of postoperative recall does not assure that episodes of awareness have not occurred during propofol-induced hypnosis.

Acoustic Stimulation↗
PubMed2001

Propofol and gastric effects of morphine.

OBJECTIVE: The purpose of this study was to evaluate whether propofol abolishes morphine-induced effects on gastric emptying and gastric tone. METHOD: The study was carried out before anesthesia in 40 patients (ASA I-II). Gastric tone was measured in 20 patients by an electronic barostat. Volume changes were thereby registered continuously in an intragastric flaccid bag with a constant preset pressure. All patients received i.v. morphine 0.1 mg x kg(-1) before the measurements and, in a randomized order, 10 of the patients also received a bolus dose of propofol 1 mg. kg-1 before morphine. Gastric emptying was studied with the paracetamol method in 20 patients. All patients received morphine 0.1 mg x kg(-1) i.v. 10 min before oral ingestion of 1.5 g paracetamol in 200 ml water and, in a randomized order, 10 of the patients also received propofol, a bolus dose of 0.3 mg x kg(-1) before morphine, followed by an infusion of 1 mg x kg(-1) x h(-1) during the whole study (2 h). RESULTS: The volume in the intragastric bag increased in all patients receiving morphine without propofol. In the group that received propofol before morphine, the volume in the intragastric bag decreased in all patients. The volume differences between the groups were statistically significant (P<0.01). There were no statistically significant differences of the AUC60, Cmax and Tmax of serum paracetamol concentrations between the morphine and propofol-morphine groups. CONCLUSION: Propofol did not abolish morphine-induced delay of gastric emptying even if propofol abolished the decrease of gastric tone induced by morphine.

Adult↗
PubMed2002

Induction and mechanism of apoptotic cell death by propofol in HL-60 cells.

BACKGROUND: Apoptosis (programmed cell death) occurs in various physiological and pathological conditions, exhibits a characteristic mechanism of intracellular sequential reaction and may be involved in determining clinical outcome. The antioxidant activity of propofol (2,6-diisopropylphenol) together with the stimulating effect of protein kinase C suggests that propofol might have the potential to modulate apoptosis. Thus, it is of both clinical interest and biomedical importance to investigate and clarify the effect and mechanism of propofol upon the intracellular reactions underlying apoptotic cell death. METHODS: The effect of propofol on apoptosis was investigated using cultured human promyelocytic leukemia HL-60 cells. This well-characterized cell line is useful for the study of apoptosis because the various biochemical steps occurring during apoptosis have been well documented. RESULTS: Treatment of HL-60 cells with propofol resulted in growth inhibition with the formation of apoptotic bodies in a concentration-dependent manner. DNA fragmentation and ladder formation was also observed in a concentration-dependent manner. Propofol treatment resulted in activation of caspase-3, -6, -8 and -9, thereby suggesting that cell surface death receptor activation of the caspase cascade mediates propofol-induced apoptosis with consequent formation of the cleaved product of Bid (a pro-apoptotic Bcl-2 family member protein) and activation of the mitochondrial pathway with cytosolic release of cytochrome c. CONCLUSION: Propofol may induce apoptosis, which is dependent on the mechanism that activates both the cell surface death receptor pathway and the mitochondrial pathway.

Anesthetics, Intravenous↗
PubMed1999

Characterization of the electrophysiological and pharmacological effects of 4-iodo-2,6-diisopropylphenol, a propofol analogue devoid of sedative-anaesthetic properties.

1. Several derivatives and analogues of the general anaesthetic 2,6-diisopropylphenol (propofol) have been recently synthesised with the aim of exploring the structure-activity relationships. 2. In the present study, the effects of one such compound, 4-iodo-2,6-diisopropylphenol (4-I-Pro), on gamma-aminobutyric acid type A (GABA(A)) receptors in vitro were compared with its in vivo effects in rodents. Human GABA(A) receptors were expressed in Xenopus oocytes, and the actions of 4-I-Pro on receptor function were compared with those of propofol by two-electrode voltage-clamp recording. 3. Similar to propofol, 4-I-Pro directly activated Cl- currents in the absence of GABA at all combinations of receptor subunits tested. However, the efficacy of 4-I-Pro in inducing direct activation of alpha1beta2gamma2S receptors was markedly less than that of propofol. 4. Similarly to propofol, 4-I-Pro potentiated in a concentration-dependent manner GABA-evoked Cl- currents measured at different GABA(A) receptor constructs. 5. As expected, intraperitoneal injection of propofol induced sedation, ataxia, and loss of the righting reflex in rats. In contrast, administration of 4-I-Pro failed to produce any of these behavioural effects. 6. Administration of 4-I-Pro to rats reduced in a dose-dependent manner the incidence of tonic-clonic seizures induced by pentylenetetrazol and induced an anticonflict effect as measured in the Vogel test. 7. Microdialysis revealed that, like propofol, administration of 4-I-Pro reduced acetylcholine release in the hippocampus of freely moving rats. 8. These results demonstrate that para-substitution of the phenol ring of propofol with iodine yields a compound that exhibits anticonvulsant and anticonflict effects, but is devoid of sedative-hypnotic and anaesthetic properties. Thus, 4-I-Pro possesses pharmacological characteristics more similar to anxiolytic and anticonvulsant drugs than to general anaesthetics.

Acetylcholine↗
PubMed2002

Propofol prevents endothelial dysfunction induced by glucose overload.

Surgical operations often induce acute hyperglycemia, which is known to affect endothelial functions. In this study, we examined the effects of propofol, a commonly used general anaesthetic, on bovine aortic endothelial cell (BAEC) dysfunction induced by glucose overload. 2 D-glucose overload (23 mM) induced an accumulation of superoxide anion (O2-), assessed by MCLA chemiluminescence, to a similar extent as that generated by 233 microU ml(-1) xanthine oxidase (XO) and 100 micro M xanthine. Propofol inhibited this accumulation with an IC50 of 0.21 micro M, whereas much higher concentrations of propofol were required to scavenge O2- generated by 250 microU ml(-1) XO and 100 microM xanthine (IC50: 13.5 micro M). 3 D-glucose overload attenuated ATP-induced NO production which was detected using diaminofluorescence-2 (DAF-2). The inhibition was reversed by propofol with an EC50 of 0.60 microM. In contrast, inhibitions caused by xanthine/XO were not altered by propofol (1 microM). 4 D-glucose overload suppressed ATP-induced Ca2+ oscillations and capacitative Ca2+ entry (CCE), which were both restored by superoxide dismutase, indicating that O2- was responsible. Propofol restored these attenuated Ca2+ oscillations and CCE with EC50 of 0.31 and 1.0 microM, respectively. 5 D-glucose overload (23 mM) increased the intracellular glucose concentration 4 fold, compared with cells exposed to 5.75 mM glucose, and 1 micro M propofol reduced this increase to 2.8 fold. 6 We conclude from these results that anaesthetic concentrations of propofol prevent the impairment of Ca2+-dependent NO production in BAEC induced by glucose overload. This effect is mainly due to the reduction of O2- accumulation, and involves, at least in part, the inhibition of cellular glucose uptake.

Animals↗
PubMed2002

A tyrosine kinase regulates propofol-induced modulation of the beta-subunit of the GABA(A) receptor and release of intracellular calcium in cortical rat neurones.

Propofol, an intravenous anaesthetic, has been shown to interact with the beta-subunit of the gamma-amino butyric acid(A) (GABA(A)) receptor and also to cause changes in [Ca2+]i. The GABA(A) receptor, a suggested target for anaesthetics, is known to be regulated by kinases. We have investigated if tyrosine kinase is involved in the intracellular signal system used by propofol to cause anaesthesia. We used primary cell cultured neurones from newborn rats, pre-incubated with or without a tyrosine kinase inhibitor before propofol stimulation. The effect of propofol on tyrosine phosphorylation and changes in [Ca2+]i were investigated. Propofol (3 microg mL(-1), 16.8 microM) increased intracellular calcium levels by 122 +/- 34% (mean +/- SEM) when applied to neurones in calcium free medium. This rise in [Ca2+]i was lowered by 68% when the cells were pre-incubated with the tyrosine kinase inhibitor herbimycin A before exposure to propofol (P < 0.05). Propofol caused an increase (33 +/- 10%) in tyrosine phosphorylation, with maximum at 120 s, of the beta-subunit of the GABA(A)-receptor. This tyrosine phosphorylation was decreased after pre-treatment with herbimycin A (44 +/- 7%, P < 0.05), and was not affected by the absence of exogenous calcium in the medium. Tyrosine kinase participates in the propofol signalling system by inducing the release of calcium from intracellular stores and by modulating the beta-subunit of the GABA(A)-receptor.

Animals↗
PubMed2001

Induction with propofol target-concentration infusion vs. 8% sevoflurane inhalation and alfentanil in hypertensive patients.

Haemodynamic parameters during an inhalation induction with 8% sevoflurane were compared with those obtained with a target-controlled infusion of propofol in 50 hypertensive patients in a prospective randomised study. Heart rate and arterial pressure were recorded continuously. End-tidal sevoflurane and nitrous oxide concentration, SpO2 and bispectral index (BIS) were also collected from the beginning of anaesthesia until 8 min after tracheal intubation. Patients either received 4 mg.l-1 target-concentration propofol or performed a vital capacity inhalation of 8% sevoflurane in a high flow of oxygen (8 l.min-1) supplemented with 50% nitrous oxide at loss of consciousness. As soon as BIS was < 60, 20 microg.kg-1 alfentanil and 0.6 mg.kg-1 rocuronium were injected and orotracheal intubation was then performed 1 min later. Thereafter, the end-tidal concentration of sevoflurane was reduced to 1.3 minimum alveolar concentration (MAC). Hypotension was defined as a 30% decrease in arterial pressure and was treated with repeated 3-mg boluses of ephedrine. When 12 mg ephedrine was unable to correct hypotension, the concentration of propofol was reduced by 1 mg.l-1 and that of sevoflurane by 0.5%. Hypotension occurred in 22 patients in the sevoflurane group and 21 in the propofol group, and hypertension occurred in two and three patients in each group, respectively. The maximal reduction in mean (SD) arterial pressure was similar in the sevoflurane (45 (4) mmHg) and propofol (41.3 (2.6) mmHg) groups, as were the ephedrine requirements (9.6 (1.1) vs. 9.1 (1.1) mg, sevoflurane vs. propofol, p > 0.05), the duration of hypotension (276 (37) vs. 292 (38) s, sevoflurane vs. propofol, p > 0.05), and the number of hypotensive episodes or anaesthetic changes and depth of anaesthesia. Nevertheless, heart rate was lower during the 8 min following tracheal intubation in the sevoflurane group. In both groups, the duration of hypotension was easily controlled either by ephedrine or by adjusting the anaesthetic concentrations. Overall, haemodynamic tolerance appears to be similar in the two techniques. Because hypotension occurred after alfentanil in most patients, this study questioned which is the best opioid dose, if any, to associate with propofol or sevoflurane for the induction in hypertensive patients.

Aged↗
PubMed1997

A comparison of propofol and other sedative use in paediatric intensive care in the United Kingdom.

The retrospective study was designed to examine the safety of propofol against other sedative agents when used by infusion for the sedation of children requiring mechanical ventilation. One-hundred-and-ninety-eight patients were recruited. One-hundred-and-six received propofol and 92 received other sedative agents for durations of 30 min to 156 days and 13 min to 11 days respectively. The mean infusion rate of propofol was 3.39 mg.kg-1.h-1. Sixty-one of the 92 patients in the nonpropofol group received midazolam at a mean infusion rate of 0.4 mg.kg-1.h-1. Forty-one patients developed clinical metabolic acidosis with five falling into the pathological range as defined. Seventeen received propofol and 24 another sedative agent. Seventy-eight percent of patients that became acidotic were under the age of three. No patients who became acidotic was noted to have lipaemic serum. Three of four patients were recorded as having lipaemic serum received propofol, however two of these patients along with the patient that received midazolam also received Intralipid. Overall mortality was similar in both sedation groups with 27 deaths being recorded. Thirteen patients received propofol. Five nonfatal adverse events occurred, three in patients that had received propofol. The findings of the survey suggest that propofol compares favourably with other sedative agents when used for sedating children in a paediatric intensive care unit.

Acidosis↗
PubMed2000

The effect of propofol on intraoperative electrocorticography and cortical stimulation during awake craniotomies in children.

Propofol has been proposed as a sedative agent during awake craniotomies. However, there are reports of propofol suppressing spontaneous epileptiform electrocorticography (ECoG) activity during seizure surgery, while others describe propofol-induced epileptiform activity. The purpose of this study was to determine if propofol interferes with ECoG and direct cortical stimulation during awake craniotomies in children. Children scheduled for awake craniotomies for resection of epileptic foci or tumours were studied. An intravenous bolus of 1-2 mg.kg-1 followed by infusion of 100-200 microgram.kg-1.min-1 of propofol was administered to induce unconsciousness. Fentanyl (0.5 microgram.kg-1) was administered incrementally to provide analgesia. After the cortex was exposed, the propofol infusion was stopped and the patient permitted to awaken. Cortical electrodes were applied. ECoG was recorded continuously on a Grass polygraph. Motor, sensory, language, and memory testing were done throughout the procedure. The cortex was stimulated with a hand-held electrode using sequential increases in voltage to map the relevant speech and motor areas. We studied 12 children (aged 11-15 years) with intractable seizures. The raw ECoG did not reveal any prolonged beta-waves associated with propofol effect. Electroencephalogram spikes due to spontaneous activity or cortical stimulation were easily detected. Cognitive, memory and speech testing was also successful. We conclude that propofol did not interfere with intraoperative ECoG during awake craniotomies. Using this technique, we were able to fully assess motor, sensory, cognitive, speech and memory function and simultaneously avoid routine airway manipulation.

Adolescent↗
PubMed2001

Propofol and midazolam in the treatment of refractory status epilepticus.

PURPOSE: To explore outcome differences between propofol and midazolam (MDL) therapy for refractory status epilepticus (RSE). METHODS: Retrospective chart review of consecutive patients treated for RSE between 1995 and 1999. RESULTS: We found 14 patients treated primarily with propofol and six with MDL. Propofol and MDL therapy achieved 64 and 67% complete clinical seizure suppression, and 78 and 67% electrographic seizure suppression, respectively. Overall mortality, although not statistically significant, was higher with propofol (57%) than with MDL (17%) (p = 0.16). Subgroup mortality data in propofol and MDL patients based on APACHE II (Acute Physiology and Chronic Health Evaluation) score did not show statistically significant differences except for propofol-treated patients with APACHE II score > or = 20, who had a higher mortality (p = 0.05). Reclassifying the one patient treated with both agents to the MDL group eliminated this statistically significant difference (p = 0.22). CONCLUSIONS: In our small sample of RSE patients, propofol and MDL did not differ in clinical and electrographic seizure control. Seizure control and overall survival rates, with the goal of electrographic seizure elimination or burst suppression rather than latter alone, were similar to previous reports. In RSE patients with APACHE II score > or = 20, survival with MDL may be better than with propofol. A large multicenter, prospective, randomized comparison is needed to clarify these data. If comparable efficacy of these agents in seizure control is borne out, tolerance with regard to hemodynamic compromise, complications, and mortality may dictate the choice of RSE agents.

APACHE↗
PubMed2000

Total intravenous anesthesia with a propofol-ketamine combination during coronary artery surgery.

OBJECTIVE: To evaluate the cardiovascular effects of a propofol-ketamine combination in patients undergoing coronary artery surgery. DESIGN: Prospective, randomized study. SETTING: Tertiary care teaching hospital, single center. PARTICIPANTS: Seventy-eight adult patients. INTERVENTIONS: Patients were randomly allocated to receive propofol-ketamine for induction and maintenance of anesthesia (n = 36) or fentanyl-enflurane (controls, n = 42). MEASUREMENTS AND MAIN RESULTS: Hemodynamics and other variables were recorded during and after surgery and for 24 hours in the intensive care unit. Before cardiopulmonary bypass (CPB), there was similar incidence of treatment for hypotension (42% of patients in both groups), tachycardia (propofol-ketamine, 6%; controls, 5%), and myocardial ischemia (propofol-ketamine, 3%; controls, 12%). In the propofol-ketamine group, there was a decreased requirement for inotropic agents after CPB (22% of patients) compared with controls (49% of patients; p = 0.02). There was a reduced incidence of myocardial infarctions (creatine kinase myocardial band >133 U/L) in the propofol-ketamine group compared with the control group (0% v 14%; p = 0.02; Fisher's exact test). Patients in the propofol-ketamine group were more likely to have their tracheas extubated within 8 hours of arrival in the intensive care unit compared with controls (33% v 7%; p = 0.01; Cochran-Mantel-Haenzel test). CONCLUSIONS: The propofol-ketamine combination was associated with a similar incidence of pre-CPB hypotension and ischemia, a decreased need for inotropes after CPB, an earlier time to tracheal extubation, and a reduced incidence of myocardial infarctions compared with controls.

Anesthesia, Intravenous↗
PubMed2001

Direct effects of propofol on myocardial and vascular tissue from mature and immature rats.

OBJECTIVE: To determine the effect of age on the direct myocardial and vascular effects of propofol in rats. DESIGN: Randomized, prospective with repeated measures. SETTING: University research laboratory. PARTICIPANTS: Myocardial and aortic tissue from 12 immature (4-week-old) and 12 mature (16-week-old) male Sprague-Dawley rats. INTERVENTIONS: Change in force of contraction was measured in isolated myocardial strips or in isolated descending thoracic aorta rings during exposure to propofol or intralipid. MEASUREMENTS AND MAIN RESULTS: Propofol produced a dose-dependent decrease in vascular tone (p < 0.05). This effect was similar for intralipid. Propofol was more potent in the younger animals (EC(50), 5.3 microg/mL [confidence interval, 2.5 to 11.1] for 4-week-old and 26.6 microg/mL [confidence interval, 6.8 to 103.7] for 16-week-old rats; p < 0.05). In contrast, propofol produced a dose-dependent decrease in contractility (p = 0.001), whereas intralipid produced no decrease in contractility. CONCLUSIONS: Although propofol does produce a dose-dependent decrease in contractility, this effect is similar at different ages. Propofol produces more direct vascular relaxation in the immature tissue. Propofol's direct cardiovascular effect and its indirect cardiovascular effects should be considered in the young and old, especially when cardiovascular reserve is limited.

Aging↗
PubMed2000

Propofol versus midazolam for conscious sedation guided by processed EEG during endoscopic retrograde cholangiopancreatography: a prospective, randomized, double-blind study.

BACKGROUND AND STUDY AIMS: Endoscopic retrograde cholangiopancreatography (ERCP) is a complex procedure, which requires appropriate sedation. The aim of this prospective, randomized, double-blind study was to compare the quality and characteristics of sedation with midazolam or propofol in patients undergoing ERCP. PATIENTS AND METHODS: A total of 32 patients undergoing ERCP were randomly allocated for sedation with propofol (n = 15) or midazolam (n = 17). Blood pressure, heart rate, and O2 saturation were monitored. Sedation was maintained at near constant levels by use of the spectral edge frequency (SEF) technique, an EEG-based method for measuring the depth of sedation. Clinical variables, patient cooperation, time to recovery, and amnesia served as outcome variables. RESULTS: There was no significant difference between the two study groups in patient characteristics. The "target SEF" was 13.6 +/- 0.7 Hz for the propofol group and 14.8 +/- 1.1 Hz for the midazolam group (n.s.). The only clinical parameter with a significant difference between the groups was the percent of time in which the heart rate deviated more than 20% from baseline for at least 2 minutes, i.e. 14.6 +/- 2.0 % for propofol and 48.2 +/- 38.0% for midazolam (P<0.01). Patient cooperation was better in the propofol group than in the midazolam group (full cooperation, 13/15 vs. 1/17, respectively; P<0.001). Patient recovery was significantly quicker in the propofol group (P<0.001). The degree of amnesia was similar in both groups; no patient in either group remembered details of the procedure. CONCLUSIONS: ERCP is better tolerated by patients sedated with propofol compared with midazolam, with a shorter recovery time and lesser hemodynamic side effects. Propofol should be considered to be the sedative drug of choice for ERCP.

Adolescent↗
PubMed2006

Propofol sedation during endoscopic procedures: safe and effective administration by registered nurses supervised by endoscopists.

BACKGROUND AND STUDY AIMS: Propofol has several attractive properties, including a rapid onset of action and rapid recovery. However, the administration of propofol sedation in the absence of anesthesiologists remains controversial. This report describes the safety profile of propofol sedation for endoscopy when administered by registered nurses under the supervision of endoscopists. PATIENTS AND METHODS: The study was conducted in the endoscopic center of a Japanese private hospital. With assistance from an anesthesiologist, a protocol for administration of propofol by registered nurses was developed. Over the past 6 years, 27,500 patients received nurse-administered propofol sedation. The safety and patient satisfaction with this sedation procedure were evaluated. RESULTS: Among the participating patients, 6.7% developed hypoxemia (Sp(O2) < 90%); 6.2% required oxygen administration via a nasal cannula. Severe hypoxemia (Sp(O2) < 85%) occurred in 121 patients (0.62%) during upper gastrointestinal endoscopy and 20 patients (0.25%) during colonoscopy, but neither mask ventilation nor endotracheal intubation was necessary. A decline in blood pressure (systolic blood pressure < 90 mm Hg) was seen in 3.5% of the colonoscopy patients and 1.2% of the upper endoscopy patients. However, hypotension was corrected immediately using an intravenous saline solution. Patients who received propofol sedation expressed overall satisfaction on a 10-point visual analogue scale (with an average of 9.4 points). Among patients who had previously received a combination of midazolam and pethidine for colonoscopy, 85% preferred propofol sedation. The mean time from the end of the procedure to full recovery was 14.6 min. CONCLUSIONS: Administration of propofol by registered nurses under the supervision of endoscopists was safe, and resulted in high rates of patient satisfaction.

Adolescent↗
PubMed2000

[Deep sedation in gastrointestinal endoscopic interventions: safety and reliability of a combination of midazolam and propofol].

BACKGROUND AND OBJECTIVE: Midazolam (M) is well known and established in endoscopic procedures for so-called conscious sedation. Propofol (P) is given during endoscopy for deep sedation. The combination of both (M/P) in endoscopic procedures is new. In this prospective study the safety of the combination was tested, in a second prospective study the combination M/P with Propofol alone was compared. PATIENTS AND METHODS: In the first study 143 patients undergoing 150 endoscopic procedures (expected > 30 min) were included. Deep sedation was induced by an i.v. bolus of 2.5 mg midazolam, followed by small doses of propofol. The sedation was performed by a second physician experienced in intensive care. In the second prospective study 64 patients undergoing two necessary endoscopic procedures were included: one deep sedation with propofol alone, the second one with combination of midazolam bolus followed by propofol. RESULTS: It was demonstrated that induction of deep sedation by an i.v. bolus of 2.5 mg midazolam, followed by small doses of propofol is safe, without undesirable side effects, e.g. respiratory or circulation depression. Recovery time increased (4 to 8 minutes) with the combination M/P, costs decreased by saving 59% propofol per minute. This may be important for longer endoscopic procedures. CONCLUSION: The combination of M/P for deep sedation during endoscopy may be useful when long procedures are expected or patients are at risk with propofol alone.

Adult↗
PubMed2002

Cost-effectiveness of propofol anesthesia using target-controlled infusion compared with a standard regimen using desflurane.

The cost-effectiveness of propofol anesthesia using target-controlled infusion (TCI) versus a standard regimen using desflurane for anesthesia maintenance was analyzed. This observational study consisted of 100 inpatients 18 to 75 years old with an American Society of Anesthesiologists physical status of I or II who were scheduled for otological surgery lasting less than four hours. Patients received one of two treatments. The desflurane-maintenance group received propofol 2-4 mg/kg and sufentanil 0.15-0.30 microg (as the citrate)/kg. A constant fresh gas flow of 1 L/min was used during maintenance of anesthesia. The propofol-maintenance group received TCI propofol and an additional infusion of sufentanil. Anesthesia was induced with 0.15-0.30 microg/kg. One blinded evaluator assessed the postoperative recovery from anesthesia for all patients. The cost of drugs and medical devices used during the intraoperative and postoperative periods was calculated. Effectiveness was defined as the absence of postoperative nausea and vomiting (PONV), while the cost-effectiveness of each procedure was the cost per PONV-free episode. The efficiency of each procedure represented the production of effectiveness per dollar invested. Chi-square and t tests, sensitivity analysis, and logistic regression were also performed. The only intergroup difference detected was the frequency of PONV occurring in the early recovery phase (11 in the desflurane group versus 2 in the propofol group). Of those patients requiring antiemetic rescue, 9 were in the desflurane group and only 2 were in the propofol group (p < 0.05). The TCI propofol regimen was more expensive than the desflurane regimen ($45 versus $28 per patient, respectively) (p < 0.001). The differential cost-effectiveness ratio was $94.7 per PONV-free episode. PONV 24 hours after surgery and patient satisfaction were similar between groups. A standard regimen of desflurane was more cost-effective than TCI propofol for anesthesia maintenance in achieving PONV-free episodes.

Adolescent↗
PubMed1991

Effect of i.v. anaesthesia with propofol on drug distribution and metabolism in the dog.

We have studied the effect of i.v. anaesthesia with propofol in the emulsion (Intralipid) formulation on drug distribution and metabolism in six dogs using dual-route administration of propranolol as a model compound. Each dog was studied on two consecutive days: day 1 awake and day 2 during propofol anaesthesia (6 mg kg-1 followed by an infusion of 0.8 mg kg-1 min-1). Propofol anaesthesia was associated with reduced intrinsic clearance by 40% (P less than 0.05) but no significant difference in systemic clearance or hepatic plasma flow. Propofol produced marked changes in drug distribution; volume of distribution (Vss) of propranolol increased 54% from 82.5 (SEM 7.3) litre awake to 127.3 (27) litre during propofol anaesthesia (P less than 0.05). This change was accompanied by an increase (P less than 0.05) in the free fraction of propranolol from 8.5 (0.7) % in awake to 14.0 (0.7) % in propofol-anaesthetized dogs. The combination of the effects of both drug clearance and protein binding resulted in a 65% decrease in the intrinsic clearance of unbound drug (P less than 0.05). In contrast with the effects of propofol on drug distribution, infusion of Intralipid alone in another group of six dogs had no significant effects on drug distribution, protein binding or drug metabolism. We conclude that propofol is a modest inhibitor of drug metabolism, but has major effects on propranolol distribution, possibly by changing plasma protein binding.

Anesthesia, Intravenous↗
PubMed1992

Hypnotic and anaesthetic interactions between midazolam, propofol and alfentanil.

We have examined interactions between midazolam, propofol and alfentanil using two end-points of light sedation (hypnosis) and anaesthesia. Quantal dose-response curves were determined in 400 female patients for the drugs individually and in combination. At the hypnotic end-point, interactions were analysed by fitting the data to a mathematical model where the response depended on the doses of the three drugs with additional terms included to describe non-additive interactions of the various combinations of the three drugs. There were significant interactions for hypnosis; the decrease in expected ED50 for the various combinations were: midazolam-propofol = 37%, midazolam-alfentanil = 46%, propofol-alfentanil = 20%, midazolam-propofol-alfentanil = 42%. Whilst all responses to the two-drug combinations were synergistic, the three-drug combination led to a response that was less than that expected from the effects of the individual agents and their two drug interactions. For anaesthesia, dose-related effects could not be demonstrated for midazolam or alfentanil when used alone. The decrease in ED50 of propofol in the presence of the other compounds was propofol-midazolam = 52%, propofol-alfentanil = 73%, propofol-midazolam-alfentanil = 82%. When comparing the different combinations, the responses varied markedly at each end-point assessed and could not be predicted from the responses of the individual agents.

Adolescent↗