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PubMed2006

Prevention of pain on injection of propofol: a comparison of remifentanil with alfentanil in children.

AIM: Propofol has a high incidence of pain on injection, particularly when a vein on the back of hand is used. Administration of lidocaine, either before or mixed with propofol remains the most widely used method to attenuate this pain. The use of opioids such as alfentanil and fentanyl has been found to decrease pain induced by propofol injection. The purpose of this study was to evaluate the effects of different doses of remifentanil and alfentanil in minimizing the pain caused by propofol. METHODS: In this randomized, double-blind, placebo-controlled study, healthy premedicated children between the age group of 5-12 years admitted for adenotonsillectomy were randomly allocated to one of 6 treatment groups. Group I: remifentanil 0.25 microg kg(-1); Group II: remifentanil 0.50 microg kg(-1); Group III: alfentanil 15 microg kg(-1); Group IV: alfentanil 20 microg kg(-1) 60 s prior to propofol mixed with 1 mL of 0.9% normal saline; Group V: lidocaine 1 mL of 1% (10 mg) added to 100 mg of propofol and Group VI: normal saline. During the injection of propofol (3 mg kg(-1)) pain perception was assessed with a four-point behavioural scale: none, mild, moderate, or severe. RESULTS: There were 52 subjects in Group I, 51 in Group II, 49 in Group III, 52 in Group IV, 52 in Group V and 52 in Group VI; 63.46% of patients in Group I, 39.21% in Group II, 38.77% in Group III, 36.53% in Group IV, 38.46% in Group V and 84.61% in Group VI experienced pain. Statistically, Groups II, III, IV and V were significantly better than placebo in the reduction of propofol pain (P<0.0001). Groups II, III and IV significantly reduced the pain in comparison with Group I (P<0.001). CONCLUSION: Pretreatment with intravenous remifentanil 0.5 microg kg(-1), alfentanil 15 microg kg(-1) and 20 microg kg(-1) were equally effective in reducing pain associated with propofol injection in children between the age group of 5-12 years.

Alfentanil↗
PubMed1991

Effect of syringe filter and i.v. administration set on delivery of propofol emulsion.

Propofol emulsion was studied to determine the effects of filtration and of passage through an i.v. administration set on drug concentration. To study syringe filter effects, propofol emulsion samples (Diprivan Injection, 10 mg/mL) were discharged through either a 5-mm filtering needle or a standard needle. To determine the effects of the i.v. administration set on propofol delivery, a diluted dispersion containing approximately 2 mg/mL was prepared from propofol emulsion and 5% dextrose injection. This formulation was siphoned into a 6-foot length of administration set tubing, from which samples were withdrawn at 0, 30, 60, and 120 minutes. Another 2-mg/mL diluted dispersion of propofol and 5% dextrose injection was placed in a glass reservoir and delivered through a 6-foot i.v. set at a rate of 1.75 mL/min, which corresponds to a low dosage rate of 0.05 mg.kg-1.min-1. Samples of the effluent were collected at 0, 5, 10, 15, 30, 60, 90, and 120 minutes. Samples collected from all three tests were assayed by using high-performance liquid chromatography. The mean propofol concentrations in the filtered and unfiltered samples were 96.05% and 96.09% of label claim, respectively, after discharge through needles; the difference was not significant. In the static study of the i.v. tubing effects, a 31.54-34.74% loss of propofol occurred after 120 min. In the study of propofol flowing through the i.v. tubing, the concentration dropped slightly in the initial sample, which was taken after the propofol was placed in the tubing. The concentration remained essentially constant for the first hour and then declined, with an overall average loss of 7.70%.(ABSTRACT TRUNCATED AT 250 WORDS)

Drug Delivery Systems↗
PubMed1988

Propofol, the newest induction agent of anesthesia.

Propofol is a rapidly acting intravenous anesthetic agent which has many advantageous kinetic properties explaining its usefulness by bolus dose for induction of anesthesia or for administration by continuous intravenous infusion. It is rapidly distributed in the body with a half-life of only around 2 min and has an efficient hepatic and extrahepatic clearance (total body clearance may exceed liver blood flow). Premedication has little effect on the already good induction characteristics of propofol. The incidence of cardiorespiratory depression appears to be higher than that of other induction agents, but, on the other hand, the absence of tachycardiac response prevents the increase in cardiac oxygen demands. In patients with cardiac disease, especially after high or repeated doses, propofol may be more depressant to the cardiovascular system than thiopentone resulting in imbalance of regional myocardial oxygen demand and supply. Recovery from propofol is rapid and clear-headed with almost no hangover effect. This makes it very suitable for out-patient anesthesia and for cardioversion. However, even with the new emulsion formulation of the drug, pain on injection is still a problem. With regard to a longer lasting combination anesthesia propofol remains an alternative to older induction agents. When given as a continuous intravenous infusion for total intravenous anesthesia or for sedation in intensive care unit propofol has shown little accumulation. Its clinical effects are predictable, consistent and recovery is rapid, independent of the dose given. Propofol has proved to be a useful induction agent regardless of the age of patients, but in the elderly there appears to exist a marked sensitivity to it. Up to now there is no evidence that propofol in emulsion drug form can produce allergic or anaphylactoid reaction more often than other induction agents in use and no severe hematological nor visceral toxicity have been reported. In the present situation, when althesin is not marketed any more due to a high frequency of anaphylactoid reactions and etomidate will have a limited use in clinical practice because of its blocking effect on adrenocortical function, propofol offers an important alternative anesthetic agent to thiopentone.

Anesthetics↗
PubMed1995

Effects of chloramphenicol on infusion pharmacokinetics of propofol in greyhounds.

To investigate the effect of chloramphenicol, a cytochrome P-450 inhibitor, on the pharmacokinetics of propofol, either chloramphenicol (50 mg/kg of body weight, IV) or saline solution was administered IV to 5 Greyhounds in randomized manner, with at least 2 weeks between trials. Thirty minutes after either chloramphenicol or saline treatment, a bolus dose of propofol (10 mg/kg, IV) was administered, followed by a 2-hour infusion of propofol (0.4 mg/kg/min, IV). Samples for determination of blood propofol concentration were collected sequentially over a 6-hour period during each trial. After termination of propofol infusion, the time to spontaneous head lift, extubation, sternal recumbency, and standing was recorded. Blood propofol concentration was determined by use of high-performance liquid chromatography. Concentration-time data were fitted to a two-compartment open pharmacokinetic model and pharmacokinetic variables were determined, using a microcomputer program for modeling and simulation of concentration-time data. The effect of chloramphenicol on the pharmacokinetics of propofol and recovery time were evaluated, using paired t-tests and Wilcoxon's test for parameters that are not normally distributed (t1/2(beta), Vd(ss), ClB). Significant (P < 0.05) effects of chloramphenicol pretreatment included increased t1/2(beta) (by 209%), and decreased ClB (by 45%), and prolonged recovery indices (by 768 to 946%). These results indicate that cytochrome P-450 metabolic pathways have an important role in propofol clearance and propofol anesthetic recovery in Greyhounds.

Anesthesia, Intravenous↗
PubMed1994

Pain on injection of propofol.

A controlled randomized double-blinded clinical study was undertaken to evaluate and compare the efficacy of three methods of preventing pain during injection of propofol on induction of anesthesia. Patients were randomly allocated to six groups: saline pretreatment, followed by induction with propofol at room temperature plus saline; lidocaine pretreatment, followed by induction with propofol at room temperature plus saline; saline pretreatment, followed by induction with propofol at a temperature of 4 degrees C plus saline; lidocaine pretreatment, followed by induction with propofol at a temperature of 4 degrees C plus saline; saline pretreatment, followed by induction with propofol at room temperature plus lidocaine 40 mg; saline pretreatment, followed by induction with propofol at a temperature of 4 degrees C plus lidocaine 40 mg. Pretreatment with lidocaine reduced the incidence of pain and discomfort significantly compared with unpretreated groups. Groups which received propofol mixed with lidocaine also showed a significant reduced incidence of pain. induction with cold 4 degrees C propofol showed no significant difference in reduction of injection pain.

Adult↗
PubMedDate not supplied

Pharmacokinetic profile of the induction dose of propofol in chronic renal failure patients undergoing renal transplantation.

STUDY OBJECTIVE: To define the pharmacokinetic profile of the induction dose of propofol in chronic renal failure patients. DESIGN AND SETTING: Determination of propofol blood concentrations after the bolus dose of 2 mg.kg-1 bw injected in 30 seconds in a peripheral vein in a group of chronic renal failure (CRF) patients and in a group of normal patients (controls). PATIENTS: 10 CRF patients (7 males, 3 females, mean age 47 +/- 8 years old, mean body weight 66 +/- 8 kg) candidates to cadaveric renal transplantation and free from major hepatic diseases (study group); 8 ASA I patients (5 males, 3 females), without major cardiorespiratory, hepatic, renal, hematologic or metabolic diseases undergoing minor elective surgical procedures lasting from 50 to 90 minutes (control group). MEASUREMENTS: a) propofol blood concentrations by means of HPLC; b) derived pharmacokinetic parameters (calculated by means of Siphar, version 4.0, Societé de informatique médicale, Simed, Paris, 1991); c) cardiovascular parameters (heart rate, central venous pressure, invasive arterial pressure). MAIN RESULTS: The decay of propofol whole blood concentrations, distribution, redistribution and elimination half lives were similar in CRF and in control patients. On the contrary, significantly different in CRF patients were propofol blood concentrations from two to ten minutes following the induction dose (lower), the area under concentration- time curve (AUC) (smaller), the mean resident time (longer), the total body clearance (greater), the volumes of distribution at steady state and during the elimination phase (larger). The larger volumes of distribution are closely correlated with the significantly lower albumin concentrations in the uremic patients. An accelerated hepatic biotransformation is one of the possible explanations for the greater total body clearance of propofol in the uraemic patients: in fact an increased glucuronyltrasferase activity and glucuronoconjugation induced by phenols has been demonstrated in uraemia. On the other hand, large volumes of distribution are often associated with elevated total body clearance. The only significant change in the cardiovascular profile was a reduction of 17 +/- 8% of the systolic blood pressure one minute after the administration of the induction dose of propofol, whereas heart rate, arterial and central venous pressures were rather stable after intubation and at skin incision: proper vascular filling before the induction of anaesthesia has probably played a crucial role in maintaining hemodynamic stability. CONCLUSIONS: From the data gathered in this study, propofol can be considered a suitable anaesthetic agent for the induction of general anaesthesia in uraemic patients. In our opinion these data could constitute a basis for future protocols of total intravenous anaesthesia with propofol in uremic patients.

Adult↗
PubMed1997

[Postoperative nausea and vomiting after gynecologic abdominal surgery--a comparison of propofol versus inhalational technique].

Propofol has been reported to reduce emesis. This study was performed to evaluate the incidence of postoperative nausea and vomiting (PONV) in gynecologic abdominal surgery patients after propofol anesthesia and inhalational anesthesia. Sixty patients were evaluated for the incidence of PONV. Thirty patients received oxygen-propofol-epidural anesthesia (propofol group) and the others were maintained with nitrous oxide-oxygen-isoflurane/sevoflurane--epidural anesthesia (inhalational group). The incidence of PONV was 33.3% in propofol group and 60% in inhalational group (P < 0.05). The means of frequency of postoperative nausea were 0.63 and 1.97 in propofol-group and inhalational group, respectively (P < 0.05). Those of postoperative vomiting were 0.17 after propofol and 1.00 following inhalational anesthesia (P < 0.01). For the gynecologic abdominal surgery patients, PONV was significantly less following intravenous anesthesia with propofol than after isoflurane or sevoflurane inhalational anesthesia. This study indicated that propofol anesthesia was useful in reducing PONV after gynecologic abdominal surgery.

Anesthesia, Epidural↗
PubMed1998

[Stereotaxy during intravenous anesthesia with propofol].

A series of 30 patients, who underwent stereotactic surgery for movement disorder under intravenous propofol anesthesia between March, 1995 and December, 1997, was retrospectively reviewed. In 28 patients with Parkinson's disease including seven juvenile cases of parkinsonism, the postoperative motor and ADL scores on the Unified Parkinson's Disease Rating Scale significantly improved. In the other two patients, one of whom had severe posttraumatic tremor and the other had cerebral palsy, the stereotactic surgery produced considerable alleviation of their symptoms. We evaluated and discussed the usefulness of intravenous propofol anesthesia in stereotaxy. Except for one patient who had an allergic reaction against propofol, none of the patients complained of intraoperative pain postoperatively. Wake-up tests were performed to record neural noise levels in 26 cases. This recording was performed under propofol anesthesia in two cases with advanced Parkinson's disease and one with cerebral palsy. In these patients, neural noise levels were recorded and were useful for identifying the target. Although the tremor disappeared under propofol anesthesia in 17 patients presenting with moderate or severe tremor, it was presented again after discontinuation of propofol. Wake-up test, therefore, made a good evaluation of Vim thalamotomy for tremor. In juvenile parkinsonian patients, three presented with dopa-induced dyskinesia (DID) during propofol infusion. In two of them, the DID emerged immediately after posteroventral pallidotomy and continued 4 or 10 hours after stereotaxy. These findings suggest that propofol possibly has an anti-parkinsonian effect. Intravenous propofol anesthesia is a useful method to use with stereotactic surgery for movement disorders.

Adult↗
PubMed2002

Similar long-term cardiovascular effects of propofol or isoflurane anesthesia during ischemia/ reperfusion in dogs.

PURPOSE: To compare the long-term functional and metabolic effects of propofol or isoflurane general anesthesia in a canine model of ischemia/reperfusion. METHODS: Using magnetic resonance (MR) techniques, we monitored both regional metabolism ((31)P MR spectroscopy) and systolic function of the heart ((1)H MR imaging) throughout a two-hour occlusion of the left anterior descending coronary artery and ten days of reperfusion. Twenty-two beagles were randomized into isoflurane and propofol general anesthesia groups (n = 10, n = 12 respectively). Contrast-enhanced MR imaging was used to measure infarct size (% of left ventricle that was necrotic) and coronary blood flow was determined using radioactively labelled microspheres. RESULTS: Cardiac metabolism, as monitored by intracellular pH and high-energy phosphate ratios, was not significantly different between the two groups throughout the protocol. Relative to propofol, isoflurane reduced the depression of left ventricular ejection fraction (EF) during the ischemic period [isoflurane 68.5% +/- 4.2%, propofol 58.3% +/- 2.0% of baseline (B); P = 0.04], propofol increased the recovery of EF at day three (isoflurane 63.9% +/- 4.3%, propofol 74.0% +/- 2.5% of B; P = 0.05). By day ten, EF in both groups was similar. Infarct sizes were also similar at day ten (isoflurane 15.7% +/- 3.0%, propofol 13.2% +/- 2.2%). Normalizing these by the region at risk (volume of tissue with low blood flow during the occlusion) to assess infarct ratios was also not significant (isoflurane 0.58% +/- 0.08%, propofol 0.54% +/- 0.07%). CONCLUSIONS: There were no significant differences between the two anesthetic groups at day ten, suggesting that any apparent dissimilarities in early cardiovascular effects were short-term only. These results indicate that isoflurane and propofol produce equivalent long-term cardiovascular effects following ischemia/reperfusion.

Anesthetics, Inhalation↗
PubMed2000

Propofol injection pain is not alleviated by pretreatment with flurbiprofen axetil, a prodrug of a nonsteroidal antiinflammatory drug.

PURPOSE: The effects of nonsteroidal antiinflammatory drugs (NSAIDs) on pain from propofol injection are controversial, partially because NSAIDs themselves cause injection pain. We evaluated the effects of flurbiprofen axetil (LFP), a prodrug of an NSAID, on pain induced by intravenous propofol injection, because LFP produces little pain on injection. METHODS: A randomized, double-blind, controlled trial was undertaken in patients who were assigned to one of three groups ( n = 50 in each). Patients received either 5 ml of saline followed approximately 10 min later by propofol mixed with 0.4 ml of saline, LFP (50 mg, 5 ml) i.v. followed by propofol mixed with 0.4 ml of saline, or 5 ml of saline followed by propofol mixed with lidocaine (40 mg, 0.4 ml). Verbal rating scores for injection pain were assessed every 10 s during propofol administration at a rate of 0.05 mg.kg(-1).s(-1). RESULTS: None of the patients complained of pain during injection of LFP or saline. Admixture of lidocaine, but not of LFP, significantly reduced the incidence of pain and the severity of pain scores during propofol injection ( P = 0.0017 and P < 0.001, respectively). CONCLUSION: Lidocaine, but not LFP, is effective for controlling pain induced by propofol injection. This result suggests that NSAIDs have little effect on pain from propofol injection.

Clinical Trial↗
PubMed2002

Comparison of heart rate changes after neostigmine-atropine administration during recovery from propofol-N2O and isoflurane-N2O anesthesia.

PURPOSE: Propofol augments the reduction of heart rate (HR) in combination with cholinergic agents and attenuates the HR response to atropine. We examined whether propofol anesthesia was associated with an increased incidence and extent of bradycardia after neostigmine-atropine administration compared with the effects of isoflurane anesthesia. METHODS: Thirty-six adult patients were randomly assigned to two groups ( n = 18 each): the propofol group patients were anesthetized with propofol (5-10 mg.kg(-1).h(-1))-(2)O-fentanyl, and the isoflurane group patients were anesthetized with isoflurane (0.5%-1.0%)-(2)O-fentanyl. When surgery was completed, anesthetics were discontinued, and then a mixture of neostigmine 0.05 mg.kg(-1) and atropine 0.02 mg.kg(-1) was injected intravenously over 20 s. Blood pressure (BP) and HR were measured noninvasively at 1-min intervals for 10 min. RESULTS: At the completion of the surgery, the average infusion rate of propofol was 6.2 +/- 1.7 mg.kg(-1).h(-1), and the average inspired concentration of isoflurane was 0.73 +/- 0.15%. Immediately before the neostigmine-atropine injections, HR and mean BP were similar in the two groups. The maximum increase in HR after the neostigmine-atropine injections was significantly less in the propofol group than in the isoflurane group (16 +/- 9 and 34 +/- 6 beats.min(-1), respectively, P < 0.01). The subsequent maximum decrease in HR was greater in the propofol group than in the isoflurane group (-9 +/- 4 and -5 +/- 4 beats.min(-1), respectively; P < 0.01). The incidence of bradycardia (HR < 50 beats.min(-1)) after neostigmine-atropine injection was greater in the propofol group than in the isoflurane group (61% and 28%, respectively; P < 0.01). CONCLUSION: We conclude that propofol anesthesia attenuates the initial increases in HR, enhances the subsequent decreases in HR, and increases the incidence of bradycardia after neostigmine-atropine injections compared with the effects of isoflurane anesthesia.

Clinical Trial↗
PubMed1994

Specificity and properties of propofol as an antioxidant free radical scavenger.

The active component of the anesthetic propofol (2,6-diisopropylphenol), which structurally resembles butylated hydroxy-toluene (BHT), a known free radical scavenger, was examined and compared to BHT with regard to its dose-dependent radical scavenging activity. Studies on the ameliorating effect of propofol in inhibiting radical production revealed that it preferentially scavenges organoradical species. In aqueous suspension it is more efficient than BHT as a free radical scavenger of riboflavin radicals and in blocking formation of malondialdehyde degradation products generated from lipid hydroperoxides of arachidonic acid. Neither propofol nor BHT showed any radical scavenging activities at concentration ranges less than 10 micrograms/ml. Propofol quenched radicals generated by photoillumination of riboflavin by 50% at 30 micrograms/ml. Under the same conditions BHT still showed no radical scavenging activity. At 50 micrograms/ml propofol the formation of malondialdehyde degradation products of arachidonic acid formed by illuminating arachidonic acid in test mixtures containing riboflavin was decreased by 38% compared to a decrease of only 24% with BHT substituted in place of propofol. The concentration of propofol required to ameliorate free radicals is approximately an order of magnitude higher than therapeutic doses of propofol used in anesthesia, suggesting that its scavenging activity during anesthesia is likely very limited.

Antioxidants↗
PubMed1996

Inhibitory effects of propofol on catecholamine secretion and uptake in cultured bovine adrenal medullary cells.

In the central and peripheral noradrenergic neurons, the balance between noradrenaline release and reuptake determines the level of noradrenaline at the synaptic cleft or the nerve ending. In the present study, we examined the effects of propofol, an intravenous general anaesthetic, on catecholamine secretion and noradrenaline uptake in cultured bovine adrenal medullary cells and on the serum noradrenaline and blood pressure in rats. In cultured adrenal medullary cells, propofol (10-50 mumol/l) concentration-dependently inhibited catecholamine secretion stimulated by carbachol. Propofol suppressed carbachol-evoked 22Na+ influx as well as 45Ca2+ influx at concentrations similar to those which suppressed the catecholamine secretion. Propofol (10-50 mumol/l) also inhibited veratridine-evoked 22Na+ influx, 45Ca2+ influx and catecholamine secretion, whereas it had little effect on the 45Ca2+ influx and catecholamine secretion induced by 56 mmol/l K+. Cultured adrenal medullary cells show [3H] noradrenaline uptake which is sensitive to imipramine. Propofol (10-50 mumol/l) significantly inhibited the imipramine-sensitive uptake of [3H] noradrenaline. In rats, intravenous administration of propofol (2.5 mg/kg) lowered serum noradrenaline and arterial blood pressure. From these findings, in spite of inhibiting noradrenaline uptake, propofol at anaesthetic concentrations (10-30 mumol/l) seems to reduce catecholamine secretion by interfering with Na+ influx through voltage-dependent Na+ channels as well as nicotinic acetylcholine receptor-associated ion channels in the adrenal medulla and, probably, in the sympathetic nervous system. This may explain the propofol-induced hypotension during anaesthesia.

Adrenal Medulla↗
PubMed1994

Propofol sequestration within the extracorporeal circuit.

Various drugs administered during cardiac anaesthesia are sequestered in the extracorporeal circuit in vitro, but it is uncertain whether this sequestration phenomenon affects plasma drug concentration in vivo. The present study was undertaken to evaluate (1) in vitro sequestration of propofol in the extracorporeal circuit and (2) whether the change in plasma propofol concentration induced by initiation of cardiopulmonary bypass in vivo can be explained by haemodilution. For the in vitro evaluation, three separate experiments with a closed circuit (membrane oxygenator, reservoir, and tubings) were performed. The pH and PCO2 of the circulating solution (a mixture of Ringer's acetate and whole blood) were maintained within the normal physiological range, and the temperature of the solution was 28 degrees C. The solution was circulated at a flow of 4 L.min-1 and propofol was added to the solution to achieve a concentration of 2 micrograms.ml-1. Serial samples were taken from the circulating solution for measurement of propofol concentration by high performance liquid chromatography. In the in vivo part of the study, 14 patients received a continuous infusion of propofol, and samples for the determination of plasma propofol concentration and blood haematocrit were taken before and five and ten minutes after initiation of cardiopulmonary bypass. In vitro, at 5 and 120 min after addition of propofol into the circulating solution, approximately 65% and 25%, respectively, of the predicted propofol level was measurable in the solution.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗
PubMed1999

Propofol does not affect the canine cardiac conduction system under autonomic blockade.

PURPOSE: To determine the effects of propofol on the cardiac conduction system in dogs with pharmacological autonomic blockade. METHODS: In eight mongrel dogs receiving 6 mg.kg-1.hr-1 propofol and vecuronium under pharmacological autonomic blockade with atropine and propranolol the infusion rates of propofol were increased from 6, (baseline), to 12, 18 and 24 mg.kg-1.hr-1 at 60-min intervals. An electrophysiological study assessed sinus rate, sinus node recovery time, corrected sinus node recovery time, intraatrial conduction time, AV nodal effective refractory period, Wenckebach cycle length and AV conduction times. Electrocardiographical variables and arterial pressures were also measured. All measurements were repeated at 30 min after the beginning of each infusion of propofol. RESULTS: Propofol did not produce direct effects on the electrophysiological or electrocardiographical variables at any infusion rates. Heart rates did not change at higher infusion rates in the presence of decreases in arterial pressures. CONCLUSION: Propofol did not affect the cardiac conduction system in the presence of autonomic blockade. Thus, the direct cardiac effects of propofol do not play a causative role in the genesis of propofol-associated bradyarrhythmias.

Anesthetics, Intravenous↗
PubMed1999

Clinical assessment of target-controlled infusion of propofol during monitored anesthesia care.

PURPOSE: To determine the plasma concentrations of propofol required to achieve different levels of sedation during monitored anesthesia care. METHODS: Sixty ASA I-II, 18-65 yr-old patients, received a target-controlled continuous iv infusion of propofol. The target plasma concentration of propofol (Cpt) was initially set at 0.4 microg x ml(-1). Two minutes after calculated equilibrium between plasma and effect-site concentrations, the Cpt of propofol was increased by 0.2 microg x ml(-1) steps until the patient showed no reaction to squeezing the trapezius. The level of sedation was assessed immediately before each increase in propofol Cpt using the Observer's Assessment of Alertness/Sedation (OAA/S) scale. RESULTS: The Cpt of propofol required to induce lethargic response to name was 1.3 microg x ml(-1) (5 degrees and 95 degrees percentiles: 1.0 - 1.8 microg x ml(-1)), to obtain response after loud and repeated calling name was 1.7 microg x ml(-1) (1.2 - 2.2 microg x ml(-1)), to obtain response after prodding or shaking was 2.0 microg x ml(-1) (1.6 - 2.6 microg x ml(-1)), to obtain response after squeezing the trapezius was 2.4 microg x ml(-1) (1.8 - 3.0 microg x ml(-1)). Patients showed no response after squeezing the trapezius at 2.8 microg x ml(-1) (2.0 - 3.6 microg x ml(-1)). Correlation between Cpt propofol and sedation scores were r = 0.76, P < 0.0001. CONCLUSIONS: Target-controlled infusion of propofol provided easy and safe management of intraoperative sedation, allowing fast and predictable deepening in the level of sedation, while minimizing systemic side effects of intravenous sedation due to the minimal risk of overdosing the drug.

Adolescent↗
PubMed1999

Oral clonidine premedication reduces induction dose and prolongs awakening time from propofol-nitrous oxide anesthesia.

PURPOSE: To evaluate whether oral clonidine premedication affects the induction dose of propofol and awakening time from epidural and propofol anesthesia. METHODS: Thirty-nine female patients (ASA I or II) were randomly allocated to receive 5 microg x kg(-1) clonidine p.o. or no clonidine 90 min before induction of anesthesia. After epidural anesthesia was achieved with lidocaine, general anesthesia was induced with continuous i.v. infusion of propofol at a rate of 50 mg x min(-1) until loss of eyelash reflex and responses to verbal commands, which were judged by a blinded observer. After a laryngeal mask airway was inserted, anesthesia was maintained with N2O 67%, O2 33% and propofol adjusted to maintain hemodynamic stability. After completion of surgery, a blinded observer recorded the time from discontinuance of propofol and N2O until the patient was awake and responsive (awakening time), and then, the laryngeal mask airway was removed. RESULTS: The induction dose of propofol in the clonidine group (1.4 +/- 0.3 mg) was less than that in the control group (1.9 +/- 0.4 mg, P < 0.05), while the awakening time of the clonidine group (470 +/- 145 sec) was longer than that of the control group (329 +/- 123 sec, P < 0.05). CONCLUSION: Premedication with 5 microg x kg(-1) clonidine p.o. reduced the induction dose of propofol, but delayed emergence from propofol anesthesia.

Adrenergic alpha-Agonists↗
PubMed1999

Rats show unimpaired learning within minutes after recovery from single bolus propofol anesthesia.

PURPOSE: To examine the learning ability of rats shortly after recovery from a bolus dose of propofol by assessing learning on a swim-to-platform task. Also, muscarinic blockade was used as a pharmacological test of whether learning shortly after propofol anesthesia resembles normal learning. METHODS: Propofol anesthetized rats (15-20 mg x kg(-1) i.v.) were trained on a swim-to-platform task five to seven minutes after recovering from surgical anesthesia and tested two to three hours later In addition, the muscarinic antagonist scopolamine hydrobromide (5 mg x kg(-1) s.c.) was given to a subgroup of rats before testing. During 10 trials, the number of times a given rat took 10 sec or longer to locate and climb onto a visible platform was tabulated and counted as errors. RESULTS: When trained shortly after recovery from the anesthetic, propofol anesthetized rats made 3.2 +/- 0.4 compared with 1.0 +/- 0.1 errors in controls (P < 0.0001). Two to three hours later both groups performed equally well. Rats trained after propofol anesthesia and given scopolamine before testing made 0.7 +/- 0.5 errors and performed as well as normal controls, 1.2 +/- 0.2 errors when subjected to the same procedures without propofol anesthesia, and better than scopolamine-treated untrained rats, 5.5 +/- 0.7 errors, (P < 0.05). CONCLUSION: Training five to seven minutes after recovery from propofol anesthesia resulted in normal retention of the swim- to-platform task. It also produced the same resistance to the disruptive effects of scopolamine as did training in rats that were not anesthetized. Thus, the ability to learn recovers rapidly after propofol anesthesia induced by a single intravenous bolus dose.

Anesthesia Recovery Period↗