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PubMed2006

Propofol, more than halothane, depresses electroencephalographic activation resulting from electrical stimulation in reticular formation.

BACKGROUND: Halothane and propofol depress the central nervous system, and this is partly manifested by a decrease in electroencephalographic (EEG) activity. Little work has been performed to determine the differences between these anesthetics with regard to their effects on evoked EEG activity. We examined the effects of halothane and propofol on EEG responses to electrical stimulation of the reticular formation. METHODS: Rats (n= 12) were anesthetized with either halothane or propofol, and EEG responses were recorded before and after electrical stimulation of the reticular formation. Two anesthetic concentrations were used (0.8 and 1.2 times the amount needed to prevent gross, purposeful movement in response to supramaximal noxious stimulation), and both anesthetics were studied in each rat using a cross-over design. RESULTS: Electrical stimulation in the reticular formation increased the spectral edge (SEF) and median edge (MEF) frequencies by approximately 1-2 Hz during halothane anesthesia at low and high concentrations. During propofol anesthesia, MEF increased at the low propofol infusion rate, but SEF was unaffected. At the high propofol infusion rate, SEF and MEF decreased following electrical stimulation in the reticular formation. CONCLUSIONS: At immobilizing concentrations, propofol produces a larger decrease than halothane in EEG responses to reticular formation stimulation, consistent with propofol having a more profound depressant effect on cortical and subcortical structures.

Anesthetics, Inhalation↗
PubMed2006

Propofol inhibits phorbol 12, 13-dibutyrate-induced, protein kinase C-mediated contraction of rat aortic smooth muscle.

BACKGROUND: Propofol induces dose-dependent vasodilation and hypotension in the clinical situation, and protein kinase C (PKC)-mediated Ca2+ sensitization plays an important role in vascular smooth muscle contraction. This study is designed to examine the effects of propofol on the active phorbol ester (phorbol 12, 13-dibutyrate; PDBu)-induced, PKC-mediated contraction of rat aortic smooth muscle. METHODS: The PDBu-induced contraction of endothelium-denuded rat aortic rings was measured in the presence or absence of PKC inhibitor, bisindolylmaleimide I, or propofol, using isometric force transducers. The PDBu-induced PKC phosphorylation of endothelium-denuded rat aortic strips was detected in the presence or absence of bisindolylmaleimide I or propofol, using Western blotting. RESULTS: PDBu, but not the inactive phorbol ester, 4-alpha-phorbol 12-myristate-13-acetate, dose-dependently induced both a slowly developing sustained contraction and PKC phosphorylation of rat aortic smooth muscle, reaching the peak level at the concentration of 10(-6) M. The PDBu (10(-6) M)-induced contraction was dose-dependently inhibited by bisindolylmaleimide I with reductions of 6.8 +/- 1.8% (P > 0.05), 39.8 +/- 8.7% (P < 0.01) and 96.7 +/- 1.4% (P < 0.01) in response to concentrations of 5 x 10(-7) M, 10(-6)x M and 5 x 10(-6) M, respectively, and by propofol with decreases of 5.2 +/- 1. 6% (P > 0.05), 9.4 +/- 1.7% (P < 0.05), 65.3 +/- 9.2% (P < 0.01) and 96.2 +/- 1.6% (P < 0.01) in response to concentrations of 5 x 10(-7) M, 10(-6) M, 5 x 10(-6) M and 10(-5) M, respectively. Both bisindolylmaleimide I and propofol also inhibited the PDBu-induced increase in the density of the phosphorylated PKC bands in a dose-dependent manner, with decreases of 6.3 +/- 2.8% (P > 0.05), 42.9 +/- 3.2% (P < 0.01) and 96.6 +/- 3.4% (P < 0.01) in response to 5 x 10(-7) M, 10(-6) M or 5 x 10(-6) M bisindolylmaleimide I, respectively, and with decreases of 4.2 +/- 2.5% (P > 0.05), 13.5 +/- 1.7% (P < 0.05), 69.5 +/- 3.5% (P < 0.01) and 95.3 +/- 4.3% (P < 0.01) in response to 5 x 10(-7) M, 10(-6) M, 5 x 10(-6) M and 10(-5) M propofol, respectively. CONCLUSION: Propofol dose-dependently inhibits PDBu-induced, PKC-mediated contraction of rat aortic smooth muscle.

Anesthetics, Intravenous↗
PubMed2004

The effect of remifentanil on cerebral blood flow velocity in children anesthetized with propofol.

BACKGROUND: Cerebrovascular stability and rapid anesthetic emergence are desirable features of a neuroanesthetic regimen. In this randomized crossover study the effect of a low-dose remifentanil infusion on cerebral blood flow velocity (CBFV) in children anesthetized with propofol was evaluated. METHODS: Twenty healthy children aged 1-6 years undergoing urological surgery were enrolled. Following face mask induction with sevoflurane, anesthesia was maintained with a standardized propofol infusion. Rocuronium was used to facilitate tracheal intubation and normothermia, and normocapnia were maintained. All children received a caudal epidural block, and a transcranial Doppler probe was placed to measure middle cerebral artery blood flow velocity (Vmca). Each patient received a remifentanil regimen of 0.5 microg x kg(-1) followed by 0.2 microg x kg(-1) x min(-1) in a predetermined order of remifentanil + propofol or propofol alone. Vmca, mean arterial pressure (MAP) and heart rate (HR) were recorded simultaneously at equilibrium with and without remifentanil. RESULTS: The combination of remifentanil and propofol caused an 8.1% decrease in MAP (P = 0.0005) and an 11.8% decrease in HR (P < 0.0001) compared with propofol alone. Vmca was not different between the two groups (P = 0.4041). CONCLUSION: The addition of remifentanil to propofol anesthesia in children causes a reduction in MAP and HR without affecting CBFV. This may imply that cerebral blood pressure autoregulation is preserved in children under propofol and remifentanil anesthesia.

Analgesics, Opioid↗
PubMed2005

Effects of pre- versus post-anaesthetic buprenorphine on propofol-anaesthetized rats.

OBJECTIVE: To compare the effect of pre- versus post-anaesthetic intramuscular (IM) buprenorphine on intermittent intravenous (IV) propofol anaesthesia in rats. ANIMALS: Twenty healthy, adult, female, ex-breeder Sprague-Dawley rats within the mass range 274-379 g. MATERIALS AND METHODS: Animals were randomly allocated to one of two groups. Group 1 (n = 10) received 9 mug buprenorphine (IM) at the start and group 2 (n = 10) received the same dose buprenorphine at the end of anaesthesia. Five animals from each group (randomly selected) received a standardized 40-minute surgical procedure (procedure 1), the remaining half, a standardized 60-minute surgical procedure (procedure 2). Induction of anaesthesia with 4% isoflurane carried in oxygen was immediately followed by IV propofol (3 mg) and intraperitoneal diazepam (500 microg). Anaesthesia was maintained using periodic IV propofol (500 microg) injected through an indwelling tail vein cannula, by an operator ignorant of the buprenorphine status. One hour after recovery from anaesthesia, the animals' level of awareness were scored by an observer ignorant of both the buprenorphine status and the total propofol dose administered. RESULTS: Buprenorphine administration at the start of anaesthesia versus administration at the end resulted in a significant reduction in the total per-kilogram requirement for propofol from a mean of 24 mg kg(-1) (+/-2.5 mg kg(-1), n = 5) to 5.5 mg kg(-1) (+/-1.1 mg kg(-1), n = 5) for procedure 1, and from a mean of 30 mg kg(-1) (+/-1.2 mg(-1), n = 5) to 16 mg kg(-1) (+/-1.0 mg kg(-1), n = 5) in procedure 2. Animals receiving buprenorphine at the start of anaesthesia demonstrated a higher level of awareness 1 hour after cessation of anaesthesia. No adverse effects were evident in either group 24 hours after recovery. CONCLUSIONS: Buprenorphine administration at the start of periodic IV propofol anaesthesia in rats resulted in a significant reduction in the total propofol requirement and significantly improved the 1-hour post-anaesthesia recovery score. Clinical relevance Besides the ethical advantage of pre-emptive analgesia, pre-anaesthetic medication with buprenorphine in rats significantly reduces the total propofol requirements for surgical anaesthesia and in this study was found to be a safe and effective method of anaesthesia.

Analgesics, Opioid↗
PubMed2006

Laryngeal mask airway insertion requires less propofol than endotracheal intubation in dogs.

OBJECTIVE: To compare the doses of propofol required for insertion of the laryngeal mask airway (LMA) with those for endotracheal intubation in sedated dogs. STUDY DESIGN: Randomized prospective clinical study. Animals Sixty healthy dogs aged 0.33-8.5 (3.0 +/- 2.3, mean +/- SD) years, weighing 2.2-59.0 (23.4 +/- 13.6, mean +/- SD) kg, presented for elective surgery requiring inhalation anaesthesia. METHODS: Animals were randomly assigned to receive either a LMA or an endotracheal tube. Pre-anaesthetic medication was intravenous (IV) glycopyrrolate (0.01 mg kg(-1)) medetomidine (10 microg kg(-1)) and butorphanol (0.2 mg kg(-1)). Repeated IV propofol injections (1 mg kg(-1) in 30 seconds) were given until LMA insertion or endotracheal intubation was achieved, when the presence or absence of laryngospasm, the respiratory rate (fr) and the total dose of propofol used were recorded. RESULTS: The total propofol dose (mean +/- SD) required for LMA insertion (0.53 +/- 0.51 mg kg(-1)) was significantly lower than for endotracheal intubation (1.43 +/- 0.57 mg kg(-1)). The LMA could be inserted without propofol in 47% of dogs; the remainder needed a single 1 mg kg(-1) bolus (n = 30). Endotracheal intubation was possible without propofol in 3.3% of the dogs, 47% needed one bolus and 50% required two injections (n = 30). The f(r) (mean +/- SD) was 18 +/- 6 and 15 +/- 7 minute(-1) after LMA insertion and intubation, respectively. CONCLUSION AND CLINICAL RELEVANCE: Laryngeal mask airway insertion requires less propofol than endotracheal intubation in sedated dogs therefore propofol-induced cardiorespiratory depression is likely to be less severe. The LMA is well tolerated and offers a less invasive means of securing the upper airway.

Anesthesia, General↗
PubMed1990

The general anesthetic propofol enhances the function of gamma-aminobutyric acid-coupled chloride channel in the rat cerebral cortex.

The effect of the general anesthetic propofol on t-[35S]butylbicyclophosphorothionate ([35S]TBPS) binding to unwashed membrane preparations from rat cerebral cortex was studied and compared to that of other general anesthetics (pentobarbital, alphaxalone) which are known to enhance GABAergic transmission. Propofol produced a concentration-dependent complete inhibition of [35S]TBPS binding, an effect similar to that induced by pentobarbital and alphaxalone, although these agents differ markedly in potency (alphaxalone greater than propofol greater than pentobarbital). The concomitant addition of propofol either with alphaxalone or pentobarbital produced an additive inhibition of [35S]TBPS binding, suggesting separate sites of action or different mechanisms of these drugs. Moreover, although bicuculline (0.1 microM) completely antagonized the propofol-induced inhibition of [35S]TBPS binding, the effect of this anesthetic was not due to a direct interaction with the gamma-aminobutyric acidA (GABAA) recognition site. In fact, propofol, like alphaxalone and pentobarbital, markedly enhanced [3H]GABA binding in the rat cerebral cortex. Finally, propofol was able to enhance [3H]GABA binding in membranes previously incubated with the specific chloride channel blocker picrotoxin. Taken together these data strongly suggest that propofol, like other anesthetics and positive modulators of GABAergic transmission, might exert its pharmacological effects by enhancing the function of the GABA-activated chloride channel.

Anesthetics↗
PubMed2006

The effect of positive end-expiratory pressure ventilation on propofol concentrations during general anesthesia in humans.

The present study investigated the effects of positive end-expiratory pressure (PEEP) on propofol concentrations in humans. Eleven patients undergoing elective surgery were enrolled in this study. Anesthesia was induced with propofol, then maintained using 60% nitrous oxide in oxygen, fentanyl 10-20 microg/kg and continuous infusion of propofol. Vecuronium was used to facilitate the artificial ventilation of the lungs. Propofol was administered to all subjects via target-controlled infusion to achieve a propofol concentration of 6.0 microg/mL at intubation and 2.0 microg/mL after intubation. Before, during and after PEEP level of 10 cmH(2)O, cardiac output (CO) and effective liver blood flow (LBF) was measured using indocyanine green as an indicator and blood propofol concentration was determined using high-performance liquid chromatography. Data are expressed as median and range. After PEEP of 10 cmH(2)O was applied, CO and effective LBF was significantly decreased from 5.5 (3.8-6.8) L/min to 4.5 (3.2-5.8) L/min (P < 0.05), 0.78 (0.65-1.21) L/min to 0.65 (0.50-0.89) L/min (P < 0.05), respectively. Propofol concentration was significantly increased from 2.21 (1.46-2.63) microg/mL to 2.45(1.79-2.89) microg/mL (P < 0.05). These data indicate that propofol concentrations can be increased by PEEP, suggesting the possibility of overdosing following PEEP.

Adult↗
PubMed1996

Inhibitory effect of propofol on sympathetic neurotransmission results in changes of plasma neuropeptide Y in rats.

1. The effects of propofol on sympathetic neurotransmission and changes of plasma level of neuropeptide Y-like immunoreactivity (NPY-ir) were investigated in rats. 2. Intraperitoneal injection of propofol into rats lowered the systemic blood pressure and plasma NPY-ir in a dose-dependent manner. 3. Decrease of plasma NPY-ir induced by propofol was not modified in adrenalectomized rats. In the activation of adrenergic neurotransmission by a ganglionic nicotinic agonist, elevation of plasma NPY-ir was also reduced by propofol indicating the direct effect on peripheral adrenergic nerve terminals. 4. Plasma level of NPY-ir reversed in parallel with the recovery of anaesthesia induced by propofol. After an intracerebroventricular injection of propofol into the rats, both the lowering of plasma NPY-ir and the induction of anaesthesia were observed. Thus, a central nervous system effect of propofol can also be considered in its effect on plasma NPY-ir. 5. The data suggest that propofol has the ability to lower plasma NPY-ir in rats through an inhibition of adrenergic neurotransmission via central nervous pathway and/or peripheral nerve terminal blockade.

Adrenalectomy↗
PubMed1995

Behavioral effects and pharmacokinetics of propofol in rats selected for differential ethanol sensitivity.

High- and low-alcohol sensitivity (HAS and LAS) rats have been selected for their differences in ethanol-induced sleep time. The rats also differ in sensitivity to pentobarbital, halothane, isoflurane, and enflurane. To determine if this sensitivity extended to propofol, the anesthetic requirements were measured. In this study, the sleep time and the tissue levels of propofol at awakening, as well as the pharmacokinetics, were evaluated. Propofol was administered intravenously. For one group of rats, sleep times were measured; blood and brain samples were taken at awakening. Blood samples were collected in another group of rats at frequent intervals from 0 to 90 min after injection. Propofol concentration of the samples was determined by gas chromatography. The pharmacokinetic analysis was performed using a nonlinear least-squares regression program. Sleep time was not different; however, blood and brain propofol levels at awakening showed a small, but significant difference between HAS and LAS rats. Propofol blood concentration-time curve data were fitted to a three-compartment model. Pharmacokinetic parameters were also not different between the rat lines. However, sleep time was 50% longer in female rats than male rats in both strains (p < 0.0001). The rates of propofol clearance were slower in female rats, because of different rates of disappearance from the second compartment. The observations suggest that the genetic selection for ethanol sensitivity selection for propofol sensitivity was not nearly as intense and presumably involves some different genes. These two central nervous system depressants would seem to differ significantly in their mechanism of action.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗
PubMed1997

Propofol-induced ataxia and hypnosis in rat lines selected for differential alcohol sensitivity.

An alcohol-sensitive rat line, selectively bred for high sensitivity to ethanol-induced motor impairment, also exhibits greater sensitivity to gamma-aminobutyric acid type A (GABAA) receptor agonists, such as benzodiazepines and barbiturates, than an alcohol-insensitive rat line. We have investigated whether this difference was also maintained for the most recent intravenous anaesthetic, propofol. Propofol (100 mg/kg, intraperitoneally) induced similar sleep times and produced identical plasma propofol concentrations in alcohol-sensitive and alcohol-insensitive rat lines. At lower doses (50 and 75, but not 25 mg/kg), propofol produced a greater motor impairment in a tilting plane test in alcohol-sensitive than alcohol-insensitive rats shortly after the injection. Binding of a convulsant, [35S]t-butylbicyclophosphorothionate, to cerebellar and cerebrocortical GABAA receptors in the presence of 2 microM GABA was similarly affected by low micromolar propofol concentrations in both rat lines, while in the absence of GABA, propofol was slightly less potent in the alcohol-sensitive than alcohol-insensitive line. These data indicate that alcohol-sensitive rats show transiently enhanced sensitivity to an ataxic, but not to a hypnotic dose of propofol, which cannot be explained by sensitivity differences to propofol in GABAA receptors determined in a binding assay using brain membrane homogenates.

Alcohol Drinking↗
PubMed2004

Metabolic effects of propofol in the isolated perfused rat liver.

Inhibitory effects of the intravenous anaesthetic propofol on mitochondrial energy metabolism have been reported by several authors. Impairment of energy metabolism is usually coupled to reduction in ATP production, which in turn is expected to lead to several alterations in cell metabolism such as stimulation of glycolysis and inhibition of gluconeogenesis. The present work aimed at finding an answer to the question of how propofol affects energy metabolism-linked parameters in the isolated perfused rat liver. In the fed state, propofol increased glycogenolysis (glucose release), glycolysis (lactate and pyruvate production) and oxygen uptake in the range between 10 and 500 microM. In the liver of fasted rats, propofol up to 100 microM increased oxygen uptake but decreased gluconeogenesis from three different substrates: lactate, alanine and glycerol. When lactate was the substrate 50% inhibition occurred at a propofol concentration of 50 microM. Propofol (100 microM) decreased the ATP content of the liver (-33.3%), increased the AMP content (+25%) and decreased the ATP/ADP and ATP/AMP ratios (49 and 45%, respectively). Most effects of propofol are probably due to impairment of oxidative phosphorylation. Particularly, the combined differential action on oxygen uptake (stimulation) and gluconeogenesis (inhibition) is strongly suggestive of an uncoupling action also under the conditions of the intact cell. This effect, in turn, is consistent with the reported high affinity of the cellular hepatic structure, especially membranes, for propofol.

Alanine↗
PubMed2004

Defining the propofol binding site location on the GABAA receptor.

The GABAA receptor is a target of many general anesthetics. The low affinity of general anesthetics has complicated the search for the location of anesthetic binding sites. Attention has focused on two pairs of residues near the extracellular ends of the M2 and M3 membrane-spanning segments, alpha1Ser270/beta2Asn265 (15' M2) and alpha1Ala291/beta2Met286 (M3). In the 4-A resolution acetylcholine receptor structure, the aligned positions are separated by approximately 10 A. To determine whether these residues are part of a binding site for propofol, an intravenous anesthetic, we probed propofol's ability to protect cysteines substituted for these residues from modification by the sulfhydryl-specific reagent p-chloromercuribenzenesulfonate (pCMBS-). pCMBS- reacted with cysteines substituted at the four positions in the absence and presence of GABA. Because propofol binding induces conformational change in the GABAAreceptor, we needed to establish a reference state of the receptor to compare reaction rates in the absence and presence of propofol. We compared reaction rates in the presence of GABA with those in the presence of propofol +GABA. The GABA concentration was reduced to give a similar fraction of the maximal GABA current in both conditions. Propofol protected, in a concentration-dependent manner, the cysteine substituted for beta2Met286 from reaction with pCMBS-. Propofol did not protect the cysteine substituted for the aligned alpha1 subunit position or the 15' M2 segment Cys mutants in either subunit. We infer that propofol may bind near the extracellular end of the betasubunit M3 segment.

4-Chloromercuribenzenesulfonate↗
PubMed1997

Effects of tiletamine/zolazepam premedication on propofol anaesthesia in dogs.

The cardiovascular and pulmonary effects of tiletamine/zolazepam, propofol and tiletamine/zolazepam plus propofol were studied in five mongrel dogs. A cannula inserted into a raised carotid artery was used to measure mean arterial pressure (MAP) and heart rate continuously and to collect arterial blood for the determination of pH, PO2, PCO2, bicarbonate and base balance. Respiratory frequency and rectal temperature were also recorded. In the two propofol groups premedication had no significant effect on the time to rejection of an endotracheal tube and the return to sternal recumbency. The MAP and heart rate increased after tiletamine/zolazepam alone and after tiletamine/zolazepam plus propofol, although propofol alone reduced MAP and transiently increased heart rate. Respiratory frequency decreased transiently in both propofol groups in association with a significant increase in PaCO2 and decrease in PaO2. The most notable change was the hypoxaemia in the tiletamine/zolazepam plus propofol group in which the PaO2 was reduced. In all the dogs given tiletamine/zolazepam alone undesirable side effects were observed, effects which also occurred during the recovery of the dogs given tiletamine/zolazepam plus propofol.

Anesthesia, Intravenous↗
PubMed2004

The dawning of a new sedative: propofol in gastrointestinal endoscopy.

BACKGROUND: Using gentler endoscopes and improved sedation, great strides have been made in enhancing patients' comfort and acceptance of endoscopic procedures. Because morbidity and mortality have been associated with benzodiazepines in endoscopic sedation, safer alternatives were sought. Propofol (2,6-diisopropylphenol), a rapid and short-acting anesthetic, initially used in the 1980's for general anesthesia induction and maintenance, is a promising candidate. METHODS: This review article examines experiences and literature references of propofol's use in endoscopic procedures. Three critical questions are posed: What are the major advantages and potential risks of propofol? When should propofol be used? Who should administer propofol, how should it be administered, and what type of monitoring is required? RESULTS: With considerable inter-patient variability, the propofol dose must be carefully titrated according to the individual patient's response. Factors influencing dosage include age, ASA class, patient's height and procedure duration. Propofol's primary risk is its narrow therapeutic range which necessitates careful patient monitoring. CONCLUSIONS: Propofol's advantages over benzodiazepines and narcotics include a more rapid onset of action, full relief of discomfort and rapid recovery to alertness without residual sedative effects or anterograde amnesia, thereby making this drug a cost-effective and, with proper monitoring, safe choice.

Procedural Sedation↗
PubMed2000

Timing of midazolam and propofol administration for co-induction of anaesthesia.

We aimed to determine the optimum timing of midazolam administration prior to propofol to achieve the maximal reduction in the dose of propofol required to induce anaesthesia. Female (ASA 1-2) patients, aged 18 to 45 years, weighing 40 to 75 kg and scheduled for gynaecological surgery were eligible for the study. Consenting patients were randomly assigned to six groups. Group 1 received saline and Groups 2 to 6 received midazolam 3 mg at 1, 2, 4, 6 or 10 minutes respectively prior to propofol (n = 20 to 22 per group) in a blinded manner. Propofol was administered i.v. over 10 seconds and flushed in with saline 5 ml. Two minutes later, the patient's response to pressure applied to the finger was determined as an index of loss of consciousness. The ED50 of propofol in each group was determined by the up-and-down method. Propofol ED50 was reduced to 34 to 67% (P < 0.001) in the midazolam treated groups. There was no significant (P = 0.14) difference in propofol ED50 among the five groups which received midazolam. Patients who received midazolam had less recollection of events surrounding induction (P < 0.001) and recalled the induction experience as being more pleasant (P = 0.03) than those who did not receive midazolam. These results indicate that midazolam may be given up to 10 minutes prior to propofol and still achieve a substantial dose reduction.

Adult↗
PubMed2002

Use of propofol infusion in Australian and New Zealand paediatric intensive care units.

Despite the risk of propofol infusion syndrome, a rare but often fatal complication of propofol infusion in ventilated children and possibly adults, propofol infusion remains in use in paediatric intensive care units (PICU). This questionnaire study surveys the current pattern of use of this sedative infusion in Australian and New Zealand PICUs. Thirty-three of the 45 paediatric intensive care physicians surveyed (73%), from 12 of the 13 intensive care units, returned completed questionnaires. The majority of practitioners (82%) use propofol infusion in children in PICU, the main indication being for short-term sedation in children requiring procedures. 39% of respondents consider propofol infusion useful in ventilated children requiring longer-term sedation. 67% of paediatric intensivists use maximum infusion doses that may be considered dangerously high (> or = 10 mg/kg/h). Nineteen per cent use propofol infusion for prolonged periods (> 72 hours). A smaller proportion (15%) of respondents indicate that they may use both higher doses and prolonged periods of infusion, a practice likely to lead to a greater chance of serious adverse events. Knowledge of local protocols for the use of propofol infusion is associated with a significantly greater level of monitoring for possible adverse events. We suggest that national guidelines for the use of propofol infusion in children should be developed. These should include clear indications and contraindications to its use, a maximum dose rate and maximum period of infusion, with a ceiling placed on the cumulative dose given and clearly stated minimum monitoring requirements.

Anesthetics, Intravenous↗
PubMed2004

Pain during injection of propofol: the effect of prior administration of ephedrine.

Propofol causes pain on intravenous injection in 28 to 90% of patients. A number of techniques have been tried to minimize propofol-induced pain, with variable results. In a randomized, double-blind, placebo-controlled trial, we compared the efficacy of ephedrine 30 microg/kg pretreatment to lignocaine 40 mg for prevention of propofol-induced pain. Ninety-three adult patients, ASA 1 and 2, undergoing elective laparoscopic cholecystectomy were randomly assigned to three groups of 31 each. Group 1 received normal saline, group 2 received lignocaine 2% (40 mg) and group 3 received 30 microg/kg ephedrine. All pretreatment drugs were made up to 2 ml. Pain at the time of propofol injection was assessed on a four-point scale: 0=no pain, 1 =mild pain, 2=moderate pain, and 3=severe pain. Twenty-seven patients (87%) of ephedrine pretreatment patients had pain during intravenous injection of propofol as compared to 24 (77%) in the normal saline group. In the lignocaine group, propofol-induced pain was observed in only 13 (42%) when compared with other study groups (P<0.05). Pretreatment with ephedrine 30 microg/kg did not attenuate pain associated with intravenous injection of propofol, nor did it improve haemodynamic stability during induction. However, pretreatment with 2% lignocaine (40 mg) was effective in attenuating propofol-associated pain.

Adolescent↗
PubMedDate not supplied

Propofol use in pediatric patients with severe cancer pain at the end of life.

This article describes the use and effectiveness of adjuvant propofol for pain control for pediatric oncology patients at the end of life. All patients experienced severe pain and agitation, not well controlled by continuous infusion opioids and benzodiazepines. Upon starting propofol, most patients had a temporary stabilization in the dose of opioids with subjective improvement in pain control, increased alertness, and improved ability to interact. Propofol infusions were continued until death in most patients. Two patients received propofol infusions at home. Subsequent increases in opioids in 6 patients and propofol in all patients were required for optimal pain control. Adverse effects included agitation in 5 patients and hallucinations in 2, which were controllable with benzodiazepines. One patient developed severe tetany, requiring propofol interruption; propofol was successfully restarted at a lower dose with an adjuvant benzodiazepine. The authors conclude that propofol is a useful and tolerable adjuvant agent for pain management in pediatric oncology patients at the end of life. It is a useful adjuvant if pain is unresponsive to continuous infusion opioids or if rapidly escalating doses of opioids are required.

Child↗