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PubMed1999

Continuous infusions of lorazepam, midazolam, and propofol for sedation of the critically ill surgery trauma patient: a prospective, randomized comparison.

OBJECTIVE: To compare the efficacy, safety, and cost of continuous infusions of lorazepam, midazolam, and propofol in a critically ill trauma/surgery patient population. DESIGN: A prospective, randomized, nonblinded, single center. SETTING: A 16-bed intensive care unit. PATIENTS: A total of 30 ventilated patients who were 18-70 yrs of age and required pharmacologic sedation. Patients with renal and/or liver failure, a history of alcohol abuse, a head injury, or in a coma were excluded. INTERVENTIONS: Patients were randomized by block design to receive lorazepam, midazolam, or propofol. Initial boluses and infusion rates were as follows: lorazepam 0.05 mg/kg, then 0.007 mg/kg/hr; midazolam 0.05 mg/kg, then 0.003 mg/kg/hr; and propofol 0.25 mg/kg, then 0.06 mg/kg/hr. Sedation was assessed and agents titrated every 5-10 mins to achieve > or =2 and <5 on the modified Ramsay scale. Once adequate response was achieved, agents were titrated to maintain the desired level of sedation. MEASUREMENTS AND MAIN RESULTS: Maintenance doses of lorazepam 0.02+/-0.01 mg/kg/hr, midazolam 0.04+/-0.03 mg/kg/hr, and propofol 2.0+/-1.5 mg/kg/hr achieved the desired level of sedation 68%, 79%, and 62% of the time, respectively. Oversedation occurred most often with lorazepam, compared with midazolam and propofol, at 14%, 6%, and 7% of the assessment times, respectively. Undersedation occurred most frequently with propofol compared with lorazepam and midazolam, at 31%, 18%, and 16% of the assessment times, respectively. The mean number of dosage changes per day was 7.8+/-4.3 for lorazepam, 4.4+/-2.9 for midazolam, and 5.6+/-6.0 for propofol (p = .91). Sedation costs per patient day (mean +/- SD) were $48+/-$76 (lorazepam), $182+/-$98 (midazolam), and $273+/-$200 (propofol) (p = .005). The potential savings, if all study patients had received lorazepam, is $14,208 compared with $8,808 if all received midazolam. CONCLUSIONS: The data suggest that lorazepam appears to be a cost-effective choice for sedation; however, oversedation may be problematic. Midazolam is the most titratable drug in our population, avoiding excessive oversedation or undersedation. Trauma patients may respond inadequately to propofol even at higher doses. Lorazepam may be the sedative of choice in critically ill trauma/surgery patients.

Adolescent↗
PubMed1998

Propofol-induced relaxation of rat mesenteric arteries: evidence for a cyclic GMP-mediated mechanism.

Experiments were designed to evaluate whether guanosine 3',5'-cyclic monophosphate (cGMP)-mediated mechanisms contribute to vasodilation via propofol in rat mesenteric resistance arteries. Ring segments were suspended in the myograph system for isometric tension recording, and responses to propofol were tested in the presence and absence of methylene blue (MB), an inhibitor of guanylate cyclase. At concentrations > or = 1 microM, propofol caused concentration-dependent relaxation of vessel rings precontracted with U46619 (a thromboxane analog). The effect was not affected by N-monomethyl-L-arginine (L-NMMA; 50 microM). MB (5 microM) reversed propofol-induced vasodilation by 30% (p < 0.001). In contrast, MB has no effect on nifedipine-inhibited vasocontraction. The propofol-induced relaxation was further tested in rings incubated in Ca2+-free solution. U46619-induced contractions were significantly reduced by propofol (40 microM) but not by nifedipine (1 microM). Propofol reduced to a similar degree the contractions obtained to exogenously added calcium chloride in the absence and the presence of MB. Furthermore, propofol (10-100 microM) increased cGMP content in cultured bovine vascular smooth-muscle cells. Soluble guanylate cyclase inhibitors, such as MB and LY83583, attenuated this effect. This investigation suggests that propofol-induced relaxations in small arteries, in addition to inhibition of calcium influx, are mediated by increases of cGMP in the smooth muscle cells.

Animals↗
PubMed2000

Low dose propofol as a supplement to ketamine-based anesthesia during intraoperative monitoring of motor-evoked potentials.

STUDY DESIGN: Motor-evoked potentials (MEPs) were analyzed using transcranial electrical stimulation during spinal surgery in patients under ketamine-based anesthesia, with and without propofol. OBJECTIVE: To investigate the effects of propofol on MEPs and ketamine-induced adverse effects during spinal surgery in patients under ketamine-based anesthesia. SUMMARY OF BACKGROUND DATA: Intraoperative monitoring of transcranial motor-evoked responses provides a method for monitoring the functional integrity of descending motor pathways. However, because these responses are sensitive to suppression by most anesthetic agents, anesthetic technique is limited during the monitoring of MEPs. Ketamine has been reported to have little effect on MEPs but may produce adverse effects such as psychedelic effect and hypertension. Recently, it has been reported that propofol may be able to inhibit ketamine-induced adverse effects. METHODS: Intraoperative monitoring of MEPs was performed in 58 patients who underwent elective spinal surgery. Anesthesia was maintained with nitrous oxide-fentanyl-ketamine without or with low-dose (1-3 mg/kg/hr) of propofol (K group; n = 34, KP group; n = 24, respectively). Transcranial stimulation with single or paired pulses or a train of three or five pulses (interstimulus interval, 2 msec) were delivered to the scalp, and compound muscle action potentials were recorded from the left and right tibialis anterior muscles. To investigate the dose effects of propofol on MEPs, propofol was administered at an infusion rate of 6, 4, and 2 mg/kg/hr and then discontinued in 14 patients. RESULTS: Results of MEPs were comparable between the K and KP groups. The incidence of postoperative psychedelic effect was significantly less in the KP group (14%) than in the K group (41%). Although propofol inhibited MEPs dose dependently, the use of a train of pulses for stimulation could overcome such inhibition. CONCLUSIONS: If a train of pulses were used for transcranial stimulation, low-dose propofol can be effectivelyused as a supplement to ketamine-based anesthesia during intraoperative monitoring of myogenic MEPs. Addition of propofol significantly reduced the ketamine-induced psychedelic effects.

Adolescent↗
PubMed1993

Propofol combined with halothane or with fentanyl/halothane does not alter the rate of CSF formation or resistance to reabsorption of CSF in rabbits.

A previous study of the cerebral effects of propofol reported that the propofol caused an initial decrease of cerebrospinal fluid (CSF) pressure and cerebral blood flow, followed by a return of CSF pressure to control values despite continued administration of propofol and continued decrease of cerebral blood flow. One explanation for the return of CSF pressure to control values is that propofol may cause an increase of the rate of CSF formation or of resistance to reabsorption of CSF. The present study was designed to examine the effects of low, moderate, and high doses of propofol, given with either fentanyl or halothane, on the rate of CSF formation and resistance to reabsorption of CSF. The rate of CSF formation and resistance to reabsorption of CSF were determined in 12 rabbits using the technique of ventriculocisternal perfusion. In the propofol-fentanyl group (n = 6), the fentanyl dose was 100 micrograms/kg followed by 20 micrograms x kg-1 x h-1 i.v., and in the propofol-halothane group (n = 6), the concentration of halothane was 0.8 to 1.0%. For both groups, the three doses of propofol were 6 mg/kg followed by 12 mg x kg-1 x h-1, 24 mg x kg-1 x h-1, and 48 mg x kg-1 x h-1 i.v., respectively. In both groups, propofol caused no significant change of the rate of CSF formation or resistance to reabsorption of CSF.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed2006

Survival of propofol infusion syndrome in a head-injured patient.

OBJECTIVE: To describe the clinical progression of an adult patient with traumatic brain injury who survived propofol infusion syndrome. DESIGN: Case report. SETTING: Tertiary care surgical intensive care unit. PATIENT: A 21-yr-old male with traumatic brain injury was administered high doses of propofol for sedation and intracranial pressure control combined with vasopressor therapy to maintain cerebral perfusion pressure >60 mmHg. He developed a significant metabolic acidosis with a lactic acid level of 10.9 mmol/L. INTERVENTIONS: Exploratory laparotomy, discontinuation of propofol infusion. MEASUREMENTS AND MAIN RESULTS: An exploratory abdominal laparotomy was negative for traumatic injury. During the procedure, the propofol infusion was considered a possible cause and was discontinued. On review, it became apparent that a combination of high-dose propofol and catecholamines were responsible for the lactic acidosis. An echocardiogram revealed severe left ventricular dysfunction and cardiomyopathy, which resolved within 19 days. CONCLUSIONS: High-dose propofol should be avoided and alternative agents should be instituted for sedation and intracranial pressure management. The use of catecholamine infusions to maintain cerebral perfusion pressure in the setting of a high-dose propofol infusion may be pharmacologically unsound and may be a triggering factor for propofol infusion syndrome. Identification of the syndrome and discontinuation of propofol resulted in complete reversal of symptoms in the case described.

Acidosis, Lactic↗
PubMed1991

A comparative study of intravenous and rectal administration of propofol in piglets.

To compare the effectiveness of propofol given intravenously and rectally, ten piglets received propofol intravenously. On the next day, the same piglets and five other piglets were given suppositories containing propofol. Serial blood samples were collected for the analysis of propofol plasma concentration. The time course of the total plasma drug concentration was fitted into a bi-exponential function using a least square fitting regression computer programme. The volume of distribution was 2.5-2.8 l.kg-1, mean elimination half-life, 23.9 min and mean clearance 0.08 l.kg-1.min-1. The mean bioavailability by the rectal route was low. In contrast to the intravenously administered propofol, none of the piglets slept when given propofol rectally, reflecting the extremely low plasma propofol concentration. In veterinary medicine, propofol would seem to be clinically valuable for inducing intravenous anaesthesia, but would be ineffective when given rectally. The findings indicate that with the dosage forms used here, propofol would be clinically ineffective if given rectally to human infants and children.

Administration, Rectal↗
PubMed1992

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

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

Adult↗
PubMed1994

Fentanyl and propofol uptake by the lung: effect of time between injections.

The effect of time between the administrations of fentanyl and propofol on the first pass uptake of propofol in the cat lung was studied using double indicator dilution technique. The pulmonary first pass uptake of propofol (mean +/- s.e. mean) was 58 +/- 6% in six cats (control group) that had received no fentanyl prior to propofol (1 mg/kg) administration. The uptake was significantly reduced to 32 +/- 3% in animals pretreated with fentanyl (1 microgram/kg) 30 seconds before propofol administration (n = 6). However, when fentanyl was administered 3 minutes (n = 6) or 10 minutes (n = 6) prior to propofol, the pulmonary uptake of propofol (45 +/- 5%, 50 +/- 7% respectively) was not significantly reduced. The results demonstrate that the ability of fentanyl to inhibit pulmonary removal of propofol depends on its time of administration prior to propofol. These data may have clinical implication with respect to timing of the preinduction opiate injection.

Animals↗
PubMed2006

Propofol acts at the sigma-1 receptor and inhibits pentazocine-induced c-Fos expression in the mouse posterior cingulate and retrosplenial cortices.

BACKGROUND: The sigma-1 receptor is functionally linked with psychotomimetic effects of various drugs. A sigma-1 receptor agonist enhances bradykinin-induced intracellular Ca(2+) concentration ([Ca(2+)]i) increase and induces c-Fos expression in a part of the brain. The aim of this study was to investigate the effects of several intravenous anaesthetics on the sigma-1 receptor. METHODS: First, using Wistar rat brains, (+)[(3)H]SKF-10,047, a selective sigma-1 receptor agonist was displaced by propofol, dexmedetomidine, droperidol, and thiopental. Second, Fura-2 loaded NG-108 cells were incubated with (+)pentazocine, a selective sigma-1 receptor agonist, and propofol and then its fluorescence was observed after stimulation with bradykinin. Third, male ICR mice received Intrafat or propofol intraperitoneally (i.p.), followed by pentazocine i.p. Brain slices were prepared and Fos-like immunoreactivity was detected using an immunohistochemical method. results: Propofol, droperidol, and dexmedetomidine displaced (+)[(3)H]SKF-10,047 binding in a concentration-dependent manner with Ki50s of 10.2 +/- 0.6, 0.17 +/- 0.03, 5.73 +/- 1.2 microM, respectively. Thiopental sodium was practically ineffective. Propofol produced a statistically significant reduction in the maximal binding capacity (Bmax) but did not affect the dissociation constant (K(d)). (+)Pentazocine significantly enhanced bradykinin-induced [Ca(2+)]i increases, but propofol did not affect it. Pentazocine induced marked Fos-LI positive cells in the posterior cingulate and retrosplenial cortices (PC/RS), which was significantly reduced by propofol. CONCLUSIONS: These results suggest that propofol may be a sigma-1 receptor antagonist, and that various effects of propofol on the brain may be mediated, at least partly, by the sigma-1 receptor.

Analgesics, Opioid↗
PubMed2004

Effects of low dose ketamine before induction on propofol anesthesia for pediatric magnetic resonance imaging.

BACKGROUND: We aimed to investigate effects of low dose ketamine before induction on propofol anesthesia for children undergoing magnetic resonance imaging (MRI). METHODS: Forty-three children aged 9 days to 7 years, undergoing elective MRI were randomly assigned to receive intravenously either a 2.5 mg x kg(-1) bolus of propofol followed by an infusion of 100 microg x g(-1) x min(-1) or a 1.5 mg x kg(-1) bolus of propofol immediately after a 0.5 mg x kg(-1) bolus of ketamine followed by an infusion of 75 microg x kg(-1) x min(-1). If a child moved during the imaging sequence, a 0.5-1 mg x kg(-1) bolus of propofol was given. Systolic and diastolic blood pressures, heart rate, peripheral oxygen saturation and respiratory rates were monitored. Apnea, the requirement for airway opening maneuvers, secretions, nausea, vomiting and movement during the imaging sequence were noted. Recovery times were also recorded. RESULTS: Systolic blood pressure and heart rate decreased significantly in the propofol group, while blood pressure did not change and heart rate decreased less in the propofol-ketamine group. Apnea associated with desaturation was observed in three patients of the propofol group. The two groups were similar with respect to requirements for airway opening maneuvers, secretions, nausea-vomiting, movement during the imaging sequence and recovery time. CONCLUSIONS: Intravenous administration of low dose ketamine before induction and maintenance with propofol preserves hemodynamic stability without changing the duration and the quality of recovery compared with propofol alone.

Adolescent↗
PubMed1995

Inhibition by propofol (2,6 di-isopropylphenol) of the N-methyl-D-aspartate subtype of glutamate receptor in cultured hippocampal neurones.

1. The effects of propofol (2,6 di-isopropylphenol) on responses to the selective glutamate receptor agonists, N-methyl-D-aspartate (NMDA) and kainate, were investigated in cultured hippocampal neurones of the mouse. Whole cell and single channel currents were recorded by patch-clamp techniques. Drugs were applied with a multi-barrel perfusion system. 2. Propofol produced a reversible, dose-dependent inhibition of whole cell currents activated by NMDA. The concentration of propofol which induced 50% of the maximal inhibition (IC50) was approximately 160 microM. The maximal inhibition was incomplete leaving a residual current of about 33% of the control response. This inhibitory action of propofol was neither voltage- nor use-dependent. 3. Analysis of the dose-response relation for whole cell NMDA-activated currents indicated that propofol caused no significant change in the apparent affinity of the receptor for NMDA. 4. Outside-out patch recordings of single channel currents evoked by NMDA (10 microM) revealed that propofol (100 microM) reversibly decreased the probability of channel opening but did not influence the average duration of channel opening or single channel conductance. 5. Whole-cell currents evoked by kainate (50 microM) were insensitive to propofol (1 microM-1 mM). 6. These results indicate that propofol inhibits the NMDA subtype of glutamate receptor, possibly through an allosteric modulation of channel gating rather than by blocking the open channel. Depression of NMDA-mediated excitatory neurotransmission may contribute to the anaesthetic, amnesic and anti-convulsant properties of propofol.

Animals↗
PubMed2005

Inhibition of persistent sodium current fraction and voltage-gated L-type calcium current by propofol in cortical neurons: implications for its antiepileptic activity.

PURPOSE: Although it is widely used in clinical practice, the mechanisms of action of 2,6-di-isopropylphenol (propofol) are not completely understood. We examined the electrophysiologic effects of propofol on an in vitro model of epileptic activity obtained from a slice preparation. METHODS: The effects of propofol were tested both on membrane properties and on epileptiform events consisting of long-lasting, paroxysmal depolarization shifts (PDSs) induced by reducing the magnesium concentration from the solution and by adding bicuculline and 4-aminopyridine. These results were integrated with a patch-clamp analysis of Na(+) and high-voltage activated (HVA) calcium (Ca(2+)) currents from isolated cortical neurons. RESULTS: In bicuculline, to avoid any interference by gamma-aminobutyric acid (GABA)-A receptors, propofol (3-100 microM) did not cause significant changes in the current-evoked, sodium (Na(+))-dependent action-potential discharge. However, propofol reduced both the duration and the number of spikes of PDSs recorded from cortical neurons. Interestingly, relatively low concentrations of propofol [half-maximal inhibitory concentration (IC(50)), 3.9 microM) consistently inhibited the "persistent" fraction of Na(+) currents, whereas even high doses (< or =300 microM) had negligible effects on the "fast" component of Na(+) currents. HVA Ca(2+) currents were significantly reduced by propofol, and the pharmacologic analysis of this effect showed that propofol selectively reduced L-type HVA Ca(2+) currents, without affecting N or P/Q-type channels. CONCLUSIONS: These results suggest that propofol modulates neuronal excitability by selectively suppressing persistent Na(+) currents and L-type HVA Ca(2+) conductances in cortical neurons. These effects might cooperate with the opening of GABA-A-gated chloride channels, to achieve depression of cortical activity during both anesthesia and status epilepticus.

Action Potentials↗
PubMedDate not supplied

Cardiovascular effects of a continuous two-hour propofol infusion in dogs. Comparison with isoflurane anesthesia.

The cardiovascular effects during 2 hours of anesthesia with either a continuous propofol infusion or isoflurane were compared in the same six healthy dogs. Dogs were randomly assigned to be anesthesized with either propofol (5 mg/kg, i.v. administered over 30 seconds, immediately followed by a propofol infusion beginning at 0.4 mg/kg/min), or isoflurane (2.0% end-tidal concentration). The propofol infusion was adjusted to maintain a light plane of anesthesia. Dogs anesthetized with propofol had higher values for systemic arterial pressure due to higher systemic vascular resistance. Dogs anesthetized with isoflurane had higher values for heart rate and mean pulmonary artery pressure. Cardiac index was not different between the two groups. Apnea and cyanosis were observed during induction of anesthesia with propofol. At the end of anesthesia the mean time to extubation for dogs anesthetized with either propofol or isoflurane was 13.5 min and 12.7 min, respectively. A continuous infusion of propofol (0.44 mg/kg/min) provided a light plane of anesthesia. Ventilatory support during continuous propofol infusion is recommended.

Anesthesia, Inhalation↗
PubMedDate not supplied

Total intravenous anesthesia in greyhounds: pharmacokinetics of propofol and fentanyl--a preliminary study.

OBJECTIVE: To evaluate concomitant propofol and fentanyl infusions as an anesthetic regime, in Greyhounds. ANIMALS: Eight clinically normal Greyhounds (four male, four female) weighing 25.58 +/- 3.38 kg. DESIGN: Prospective experimental study. METHODS: Dogs were premedicated with acepromazine (0.05 mg/kg) by intramuscular (i.m.) injection. Forty five minutes later anesthesia was induced with a bolus of propofol (4 mg/kg) by intravenous (i.v.) injection and a propofol infusion was begun (time = 0). Five minutes after induction of anesthesia, fentanyl (2 microg/kg) and atropine (40 microg/kg) were administered i.v. and a fentanyl infusion begun. Propofol infusion (0.2 to 0.4 mg/kg/min) lasted for 90 minutes and fentanyl infusion (0.1 to 0.5 microg/kg/min) for 70 minutes. Heart rate, blood pressure, respiratory rate, end-tidal carbon dioxide, body temperature, and depth of anesthesia were recorded. The quality of anesthesia, times to return of spontaneous ventilation, extubation, head lift, and standing were also recorded. Blood samples were collected for propofol and fentanyl analysis at varying times before, during and after anesthesia. RESULTS: Mean heart rate of all dogs varied from 52 to 140 beats/min during the infusion. During the same time period, mean blood pressure ranged from 69 to 100 mm Hg. On clinical assessment, all dogs appeared to be in light surgical anesthesia. Mean times (+/- SEM), after termination of the propofol infusion, to return of spontaneous ventilation, extubation, head lift and standing for all dogs were 26 +/- 7, 30 +/- 7, 59 +/- 12, and 105 +/- 13 minutes, respectively. Five out of eight dogs either whined or paddled their forelimbs in recovery. Whole blood concentration of propofol for all eight dogs ranged from 1.21 to 6.77 microg/mL during the infusion period. Mean residence time (MRTinf) for propofol was 104.7 +/- 6.0 minutes, mean body clearance (Clb) was 53.35 +/- 0.005 mL/kg/min, and volume of distribution at steady state (Vdss) was 3.27 +/- 0.49 L/kg. Plasma concentration of fentanyl for seven dogs during the infusion varied from 1.22 to 4.54 ng/mL. Spontaneous ventilation returned when plasma fentanyl levels were >0.77 and <1.17 ng/mL. MRTinf for fentanyl was 111.3 +/- 5.7 minutes. Mean body clearance was 29.1 +/- 2.2 mL/kg/min and Vdss was 2.21 +/- 0.19 L/kg. CONCLUSION AND CLINICAL RELEVANCE: In Greyhounds which were not undergoing any surgical stimulation, total intravenous anesthesia maintained with propofol and fentanyl infusions induced satisfactory anesthesia, provided atropine was given to counteract bradycardia. Despite some unsatisfactory recoveries the technique is worth investigating further for clinical cases, in this breed and in mixed breed dogs.

Anesthetics, Intravenous↗
PubMed1999

A clinical trial of propofol vs midazolam for procedural sedation in a pediatric emergency department.

OBJECTIVE: To compare the effectiveness, recovery time from sedation, and complication rate of propofol with those of midazolam when used for procedural sedation in the pediatric emergency department (PED). METHODS: A prospective, blinded, randomized, clinical trial comparing propofol and midazolam was conducted in the PED of a tertiary pediatric center. Eligible patients were aged 2-18 years with isolated extremity injuries necessitating closed reduction. All patients received morphine for pain, then were randomized to receive propofol or midazolam for sedation. Vital signs, pulse oximetry, and sedation scores were recorded prior to sedation and every 5 minutes thereafter until recovery. Recovery time, time from cast completion to discharge, and other time intervals during the PED course and all sedation-related complications were also recorded. RESULTS: Between August 1996 and October 1997, 91 patients were enrolled. Demographic data, morphine doses, and sedation scores were similar between the propofol and midazolam groups. Mean +/- SD recovery time for the propofol group was 14.9+/-11.1 minutes, compared with 76.4+/-47.5 minutes for the midazolam group, p<0.001. Mild transient hypoxemia was the most significant complication, occurring in 5 of 43 (11.6%) patients given propofol and 5 of 46 (10.9%) patients given midazolam (odds ratio 1.08, 95% CI = 0.24 to 4.76). CONCLUSION: In this study, propofol induced sedation as effectively as midazolam but with a shorter recovery time. Complication rates for propofol and midazolam were comparable, though the small study population limits the power of this comparison. Propofol may be an appropriate agent for sedation in the PED; however, further study is necessary before routine use can be recommended.

Adolescent↗
PubMed2004

An initial investigation of bispectral monitoring as an adjunct to nurse-administered propofol sedation for colonoscopy.

BACKGROUND AND AIMS: Bispectral (BIS) monitoring has been used to evaluate depth of sedation in intensive care and surgical patients. We sought to explore its utility as a monitoring device for nurse-administered propofol sedation (NAPS) during colonoscopy. METHODS: Fifty consecutive patients (ASA I or II) receiving NAPS for outpatient colonoscopy were evaluated. BIS scores, sedation scores, and propofol dosing were correlated. The nurses assessed the usefulness of BIS by questionnaire. RESULTS: The mean (SD) dose of propofol required to produce a BIS value </= 60 was 109.4 (43.9) mg and an Observer's Assessment of Alertness/Sedation (OAA/S) score of 1 (deep sedation) was 91.4 (44.8) mg (p < 0.0001). The mean times required to achieve BIS values </= 60 (188 +/- 147.1 s) and </= 70 (164.3 +/- 95.1 s) were significantly longer than the mean time required to achieve an OAA/S of 1 (117.4 +/- 93.0 s, p= 0.0007). Similarly, during the recovery phase, there was a lag time of 197.9 s between mean (SD) time required from the last dose of propofol to an OAA/S of 5 (372.1 +/- 197.1 s) and the mean (SD) time required from the last dose of propofol to a BIS value >/= 90 or return to baseline (570 +/- 279.9 s, p < 0.0001). The mean (SD) BIS value in the maintenance phase of sedation was 58.9 (8.53), with a range of 22-88. Nurses administering propofol rated the usefulness of BIS at a mean of 2.85 (maximum usefulness scored as 4) in guiding the dosing of propofol sedation during the maintenance phase of sedation. No patient required mask ventilation or endotracheal intubation. CONCLUSIONS: The BIS index in its current version is not useful in titrating boluses of propofol to an adequate level of sedation, because there is a substantial lag time between decrease of BIS scores to <70 and OAA/S scores indicative of deep sedation. There is also a substantial lag time between recovery of alertness and return of BIS scores to normal. A controlled trial of whether BIS values can assist in avoiding unnecessary propofol dosing during the maintenance phase of sedation appears warranted.

Adult↗
PubMed2005

Effects of intrathecal 6-hydroxydopamine, alpha1 and alpha2 adrenergic receptor antagonists on antinociception of propofol in mice.

AIM: To investigate the relationship between spinal cord norepinephrine, alpha1 and alpha2 adrenergic receptors and antinociception of propofol in mice. METHODS: Kunming mice were used. Antinociceptive tests were investigated with the tail-immersion test and the acetic acid-induced writhing test. The effects of subcutaneous (sc), intrathecal (ith) and intracerebroventricular (icv) injection propofol on pain threshold were observed. The influences of pretreatment with ith 6-hydroxydopamine, alpha1R antagonist prazosin, or alpha2R antagonist yohimbine on the antinociception of propofol were studied. RESULTS: Significant antinociception was produced by propofol (25, 50 mg/kg, sc) and propofol (20, 40 microg, ith) in tail-immersion test and acetic the acid-induced writhing test (P<0.05 or P<0.01). Icv propofol (10, 20, and 40 microg) did not produce any effect on pain threshold in mice (P>0.05). The 6-hydroxydopamine (5 and 10 microg), prazosin (5 and 10 microg), or yohimbine (5 and 10 microg) ith alone did not affect basal tail-flick latency (TFL) in conscious mice, but significantly reduced the TFL as measured by tail-immersion test in propofol (50 mg/kg, sc)-treated mice, compared with basal TFL and vehicle groups (P<0.05 or P<0.01). CONCLUSION: The spinal cord is a target of propofol antinociception. In mice propofol antinociception is partly mediated by spinal norepinephrine, alpha1R and alpha2R.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed2004

Propofol-block of SK channels in reticular thalamic neurons enhances GABAergic inhibition in relay neurons.

The GABAergic reticular thalamic nucleus (RTN) is a major source of inhibition for thalamocortical neurons in the ventrobasal complex (VB). Thalamic circuits are thought to be an important anatomic target for general anesthetics. We investigated presynaptic actions of the intravenous anesthetic propofol in RTN neurons, using RTN-retained and RTN-removed brain slices. In RTN-retained slices, focal and bath application of propofol increased intrinsic excitability, temporal summation, and spike firing rate in RTN neurons. Propofol-induced activation was associated with suppression of medium afterhyperpolarization potentials. This activation was mimicked and completely occluded by the small conductance calcium-activated potassium (SK) channel blocker apamin, indicating that propofol could enhance RTN excitability by blocking SK channels. Propofol increased GABAergic transmission at RTN-VB synapses, consistent with excitation of presynaptic RTN neurons. Stimulation of RTN resulted in synaptic inhibition in postsynaptic neurons in VB, and this inhibition was potentiated by propofol in a concentration-dependent manner. Removal of RTN resulted in a dramatic reduction of both spontaneous postsynaptic inhibitory current frequency and propofol-mediated inhibition of VB neurons. Thus the existence and activation of RTN input were essential for propofol to elicit thalamocortical suppression; such suppression resulted from shunting through the postsynaptic GABA(A) receptor-mediated chloride conductance. The results indicate that propofol enhancement of RTN-mediated inhibitory input via blockade of SK channels may play a critical role in "gating" spike firing in thalamocortical relay neurons.

Action Potentials↗