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PubMed1994

Propofol infusion and the suppression of consciousness: the EEG and dose requirements.

We have used Median Power Frequency (MPF) to study changes in the electroencephalogram during propofol infusions in 52 women about to undergo gynaecological surgery. Patients were allocated to receive propofol by one of nine different manually-controlled infusion schemes designed to achieve and maintain a stable blood propofol concentration between 1.0 and 6.0 micrograms ml-1, covering a range of states between conscious sedation and full anaesthesia. We recorded the changes in MPF and the response to clinical signs of loss of consciousness at these different doses and concentrations of propofol. Using probit analysis, we derived MPF values corresponding to 50% and 95% suppression of response to verbal (9.3 Hz and 6.8 Hz), eyelash (8.9 Hz and 6.7 Hz) and venepuncture (5.7 Hz and 3.0 Hz) stimuli. Likewise, we obtained dose and concentration requirements for propofol to suppress these stimuli. The mean (95% confidence intervals) ED50 (5.8 (3.5-6.8) mg kg-1 h-1) and ED95 (8.3 (7.1-16.9) mg kg-1 h-1) propofol doses for suppression of consciousness were similar to the values for suppression of the eyelash reflex (6.2 (5.3-6.8) mg kg-1 h-1 and 8.6 (7.8-10.8) mg kg-1 h-1, respectively). The EC50 for loss of consciousness was a propofol concentration of 2.3 (1.8-2.7) micrograms ml-1 and for 50% suppression of MPF was 3.1 (2.7-3.5) micrograms ml-1. The dose required for 50% suppression of MPF was 7.1 (6.2-8.0) mg kg-1 h-1. After 30 min, at blood propofol concentrations > 4.0 micrograms ml-1, consistent with stable anaesthesia, the mean MPF was 5.6 (4.5-6.3) Hz.

Adolescent↗
PubMed1995

Human cytochrome P450 mono-oxygenase system is suppressed by propofol.

We have studied the effect of propofol on the cytochrome P450-dependent mono-oxygenase system in human liver microsomes by assaying mono-oxygenase activities toward specific cytochrome P450 isoform test substrates, aniline, 7-ethoxycoumarin, benzphetamine and benzo(a) pyrene. Propofol inhibited benzo(a)pyrene hydroxylation to a greater extent than the oxidative metabolism of the other test substrates, even at 0.05 mmol litre-1. The degrees of inhibition of benzphetamine N-demethylation and 7-ethoxy-coumarin O-de-ethylation were similar, while aniline hydroxylation was least affected by propofol. Spectral analysis showed that propofol competed with carbon monoxide for binding to the haem moiety of haemoprotein in the P450 enzyme. The variable inhibition observed may be caused by the differential binding of propofol to P450 isoforms. Propofol 0.05-1.0 mmol litre-1 exhibited a concentration-dependent inhibitory effect on human cytochrome P450 2E1, 2B1 and 1A1. These inhibitory actions of propofol on human liver microsomal enzymes in vitro suggest that potential drug interactions may exist between propofol and other drugs administered clinically.

Aniline Compounds↗
PubMed1995

The P300 event-related potential during propofol sedation: a possible marker for amnesia?

We have studied the effects of conscious sedation with propofol on long latency components of the auditory event-related potential (ERP) in 10 normal volunteers (aged 21-41 yr) receiving propofol 75 micrograms kg-1 min-1 i.v. We examined the effects of propofol on ERP amplitudes and latencies, and their relationship to delayed recognition performance using a verbal memory test, a selective attention task (button pushing) and serum concentrations of propofol. During infusion of propofol, subjects were mildly sedated, oriented and readily responsive to verbal commands. ERP were recorded from monopolar FZ, CZ and PZ electrodes. We used a standard paradigm requiring selective attention to randomly occurring stimuli associated with a task (button push). The peak-to-peak amplitudes and latencies of the N2 and P3 waves were obtained before and during infusion, and 15, 100 and 170 min after infusion. Propofol produced a 70% decrease in the amplitude of P3 (P < 0.0001) from baseline and a 50% increase in reaction time. The differential response to target compared with non-target stimuli was maintained during infusion for both N2 and P3. Memory performance correlated more strongly with changes in P3 amplitude (r = 0.59) than with serum propofol concentrations (r = -0.07), although this correlation with memory did not reach statistical significance (P = 0.08). We conclude that P3 amplitude was profoundly affected by propofol given in sedative concentrations.

Adult↗
PubMed1997

Inhalation induction with sevoflurane: a double-blind comparison with propofol.

We conducted a randomized, double-blind comparison of 8% sevoflurane and propofol as induction agents for day-case cystoscopy in 102 patients. All patients received an i.v. cannula and breathed oxygen 5 litre min-1. Anaesthesia was induced with propofol i.v. or inhalation of 8% sevoflurane and 10% Intralipid (as a placebo) i.v., delivered by a blinded observer. Anaesthesia was maintained in all patients with 2% sevoflurane via a face mask. Induction of anaesthesia with sevoflurane was significantly slower compared with propofol (mean 84 (SD 24) s vs 57 (11) s), but was associated with a lower incidence of apnoea (16% vs 65%) and a shorter time to establish spontaneous ventilation (94 (34) s vs 126 (79) s). Induction complications were uncommon in each group but the transition to maintenance was smoother with sevoflurane and was associated with less hypotension compared with propofol. Emergence from anaesthesia induced with sevoflurane occurred significantly earlier compared with propofol (5.2 (2.2) min vs 7.0 (3.2) min) and anaesthetic induction was also significantly cheaper with sevoflurane. According to a postoperative questionnaire, the majority of patients found both anaesthetic techniques acceptable. Nevertheless, significnatly more patients (14%) rated induction with sevoflurane as unpleasant compared with propofol (0) and significantly more patients (24%) would not choose sevoflurane induction compared with propofol (6%). This phenomenon may have been related to the particular patient population studied, however. Inhalation induction with 8% sevoflurane would appear to offer several objective advantages compared with induction with propofol in day-case patients, although a significant minority may dislike this technique.

Adult↗
PubMed1997

Propofol and bradycardia: causation, frequency and severity.

As part of the development of a model for the study of adverse events, we have investigated the risk of bradycardia with propofol. A systematic search for any type of report, published and unpublished, was made to review the evidence that propofol increases the risk of bradycardia, asystole and death from bradycardic events. Quantitative and qualitative analyses of data with different strengths of evidence were performed. Sixty-five published and 187 spontaneous reports to drug monitoring centres described with different strength of evidence a biological basis for propofol-induced bradycardia, 1444 bradycardias, 86 asystoles and 24 deaths. In controlled clinical trials, propofol significantly increased the risk of bradycardia compared with other anaesthetics (number-needed-to-harm 11.3 (95% confidence interval 7.7-21)). In paediatric strabismus surgery the number-needed-to-harm was 4.1 (3-6.7). One of 660 patients undergoing propofol anaesthesia had an asystole. The risk of bradycardia-related death during propofol anaesthesia was estimated to be 1.4 in 100,000. Data from the phase IV study of propofol did not agree with data from controlled studies. Propofol carries a finite risk for brady-cardia with potential for major harm. Study of adverse events should be made with systematically searched data and, in contrast with study of efficacy, not restricted to randomized, controlled trials.

Adverse Drug Reaction Reporting Systems↗
PubMed1998

Antioxidant effects of propofol in human hepatic microsomes: concentration effects and clinical relevance.

Propofol is known to possess antioxidant properties. There is controversy regarding the mechanisms by which the drug produces its antioxidant effects and the significance of these effects in relation to plasma concentrations of propofol in clinical practice. We studied the effects of increasing concentrations of Intralipid, propofol, butylated hydroxytoluene (BHT) and a vitamin E analogue (Trolox C) in 0.9% saline on non-enzymic and enzymic lipid peroxidation in human hepatic microsomes, and on concentrations of antioxidant enzymes in a Hep G2 cell line. Propofol showed significant inhibition of lipid peroxidation, but was less potent than BHT or Trolox C. IC50 values for non-enzymic and enzymic lipid peroxidation were mean 9.47 (SD 0.86) and 7.39 (0.84) mumol litre-1 for propofol, 1.30 (0.57) and 0.32 (0.02) mumol litre-1 for BHT and 2.34 (0.68) and 0.35 (0.04) mumol litre-1 for Trolox C, respectively. The antioxidant activities of propofol were substantially retained in the presence of up to 30 g litre-1 of human serum albumin. Propofol at concentrations of up to 100 mumol litre-1 had no significant effect on the activities of antioxidant enzymes. Clinically relevant concentrations of propofol produced significant inhibition of both enzymic and non-enzymic lipid peroxidation in hepatic microsomal preparations, possibly as a result of accumulation in lipophilic environments. Measurement of antioxidant effects of drugs in aqueous media may have little relevance to their effects in protecting against lipid peroxidation in biological systems.

Anesthetics, Intravenous↗
PubMed1998

Cerebrospinal fluid concentrations of propofol during anaesthesia in humans.

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

Adult↗
PubMed1999

Coating of extracorporeal circuit with heparin does not prevent sequestration of propofol in vitro.

Propofol is sequestered in extracorporeal circuits, but the factors responsible for the phenomenon are mostly unknown. We have compared two extracorporeal circuits (oxygenators, reservoirs and tubings) coated with heparin with two corresponding uncoated circuits for their capacity to sequester propofol in vitro. Three experiments were conducted with each circuit. The circuit was primed with a mixture of Ringer's acetate solution and whole blood, and the study conditions (pump flow, temperature, pH) were standardized. Propofol was added to the solution to achieve a concentration of 2 micrograms ml-1. These studies were followed with concentrations of 10- and 100-fold to assess possible saturation of propofol binding. Serial samples were obtained from the circulating solution for measurement of propofol concentration. Propofol concentrations decreased to 22-32% of the initial predicted concentration of 2 micrograms ml-1 in the circuits (no significant difference between circuits). With greater concentrations, the circuits did not become saturated with propofol, even with the highest predicted concentration of 200 micrograms ml-1. We conclude that propofol was sequestered in extracorporeal circuits in vitro, irrespective of coating the circuit with heparin.

Adhesiveness↗
PubMed2000

Effects of protein binding on the placental transfer of propofol in the human dually perfused cotyledon in vitro.

The placental transfer of propofol was investigated using the in vitro dually perfused cotyledon model of the human placenta, and the effects of protein binding in the foetal perfusate were examined. Both maternal and foetal circulations were perfused in a single-pass mode and > 30 min of stabilization was allowed before adding propofol and antipyrine to the maternal perfusate. The placental clearances of propofol were significantly increased by the augmented albumin concentrations in the foetal perfusate (1.68 (SD 0.68), 3.08 (1.55), 4.79 (1.76), 5.75 (1.89) and 7.03 (1.46) ml h-1 g-1 at the albumin concentrations of 4.4, 11, 22, 33 and 44 g litre-1, respectively). Although the total propofol concentration in the foetal vein increased significantly with increasing albumin concentration, the concentration of free propofol remained unchanged. These results indicate that binding to foetal albumin is a determining feature in the control of the placental transfer of propofol, and that the pharmacological effects of propofol on the foetus can be expected to be fairly constant and predictable from the maternal propofol concentration.

Albumins↗
PubMed2001

Clonidine decreases propofol requirements during anaesthesia: effect on bispectral index.

Assessment of the effect of clonidine on depth of anaesthesia is difficult because clonidine combines analgesic, sedative and direct haemodynamic effects. We thus evaluated the influence of clonidine on the bispectral index (BIS) and its potential dose-sparing effect on propofol. After induction of anaesthesia with target-controlled infusion of propofol and obtaining an unchanged bispectral index (pre-BIS), clonidine 4 microg kg(-1) or placebo was administered randomly to 50 patients in a double-blind manner. Subsequently, if there was a decrease in BIS we reduced the target concentration of propofol until pre-BIS was reached. The pre-BIS was maintained and a remifentanil infusion was added during surgery. The courses of the BIS, heart rate and blood pressure were recorded and the total amounts of intra-operative propofol and remifentanil were determined. Assessment of implicit memory during anaesthesia was performed with an auditory implicit memory test consisting of item sequences. Administration of clonidine resulted in a decrease in the BIS from 45 (SD 4) to 40 (6) (P<0.001), which allowed a reduction of propofol target concentration from 3.3 (0.6) to 2.7 (0.7) microg ml(-1) (P<0.001) and measured propofol concentration from 2.9 (0.6) to 2.5 (0.7) kg ml(-1) (P=0.009) in order to maintain the pre-BIS value. During subsequent surgery, propofol requirements were reduced by 20% (P=0.002) in the clonidine group and a similar amount of remifentanil was used in each group. The increase in anaesthetic depth given by clonidine can therefore be measured with bispectral EEG analysis and allows reduction of the propofol dose to achieve a specific depth of anaesthesia.

Adjuvants, Anesthesia↗
PubMed2003

Early recovery after remifentanil-pronounced compared with propofol-pronounced total intravenous anaesthesia for short painful procedures.

BACKGROUND: We compared recovery from high-dose propofol/low-dose remifentanil ('propofol-pronounced') compared with high-dose remifentanil/low-dose propofol ('remifentanil-pronounced') anaesthesia. METHODS: Adult patients having panendoscopy, microlaryngoscopy, or tonsillectomy were randomly assigned to receive either propofol-pronounced (propofol 100 microg x kg(-1) min(-1); remifentanil 0.15 microg x kg(-1) min(-1)) or remifentanil-pronounced (propofol 50 microg x kg(-1) min(-1); remifentanil 0.45 microg x kg(-1) min(-1)) anaesthesia. In both groups, the procedure was started with remifentanil 0.4 microg x kg(-1), propofol 2 mg x kg(-1), and mivacurium 0.2 mg x kg(-1). Cardiovascular measurements and EEG bispectral index (BIS) were recorded. To maintain comparable anaesthetic depth, additional propofol (0.5 mg x kg(-1)) was given if BIS values were greater than 55 and remifentanil (0.4 microg x kg(-1)) if heart rate or arterial pressure was greater than 110% of pre-anaesthetic values. RESULTS: Patient and surgical characteristics, cardiovascular measurements, and BIS values were similar in both groups. There were no differences in recovery times between the groups (time to extubation: 12.7 (4.5) vs 12.0 (3.6) min, readiness for transfer to the recovery ward: 14.4 (4.4) vs. 13.7 (3.6) min, mean (SD)). CONCLUSIONS: In patients having short painful surgery, less propofol does not give faster recovery as long as the same anaesthetic level (as indicated by BIS and clinical signs) is maintained by more remifentanil. However, recovery times were less variable following remifentanil-pronounced anaesthesia suggesting a more predictable recovery.

Adolescent↗
PubMed2004

Sequential effects of propofol on functional brain activation induced by auditory language processing: an event-related functional magnetic resonance imaging study.

BACKGROUND: We have investigated the effect of propofol on language processing using event-related functional magnetic resonance imaging (MRI). METHODS: Twelve healthy male volunteers underwent MRI scanning at a magnetic field strength of 3 Tesla while performing an auditory language processing task. Functional images were acquired from the perisylvian cortical regions that are associated with auditory and language processing. The experiment consisted of three blocks: awake state (block 1), induction of anaesthesia with 3 mg kg(-1) propofol (block 2), and maintenance of anaesthesia with 3 mg kg(-1) h(-1) propofol (block 3). During each block normal sentences and pseudo-word sentences were presented in random order. The subjects were instructed to press a button to indicate whether a sentence was made up of pseudo-words or not. All subjects stopped responding during block two. The data collected before and after the subjects stopped responding during this block were analyzed separately. In addition, propofol plasma concentrations were measured and the effect-site concentrations of propofol were calculated. RESULTS: During wakefulness, language processing induced brain activation in a widely distributed temporofrontal network. Immediately after unresponsiveness, activation disappeared in frontal areas but persisted in both temporal lobes (block 2 second half, propofol effect-site concentration: 1.51 microg ml(-1)). No activation differences related to the task were observed during block 3 (propofol effect-site concentration: 4.35 microg ml(-1)). CONCLUSION: Our findings suggest sequential effects of propofol on auditory language processing networks. Brain activation firstly declines in the frontal lobe before it disappears in the temporal lobe.

Acoustic Stimulation↗
PubMed2004

Effects of halothane, sevoflurane and propofol on left ventricular diastolic function in humans during spontaneous and mechanical ventilation.

BACKGROUND: There is limited knowledge of the effects of anaesthetics on left ventricular (LV) diastolic function in humans. Our aim was to evaluate these effects in humans free from cardiovascular disease. METHODS: Sixty patients (aged 18-47 yr) who had no history or signs of cardiovascular disease were randomized to receive general anaesthesia with halothane, sevoflurane or propofol. Echocardiography was performed at baseline and during spontaneous respiration at 1 minimum alveolar concentration (MAC) of the inhalational agents or propofol 4 microg ml(-1) (step 1), and repeated during positive-pressure ventilation with 1 and 1.5 MAC of the inhalational agents or with propofol 4 and 6 microg ml(-1) (steps 2a and 2b). Analysis of echocardiographic measurements focused on heart rate corrected isovolumic relaxation time (IVRT(c)) and early diastolic peak velocity of the lateral mitral annulus (E(a)). RESULTS: IVRT(c) decreased from baseline to step 1 in the halothane group (82 [95% CI, 76-88] ms and 74 [95% CI, 68-80] ms respectively; P=0.02), remained stable in the sevoflurane group (78 [95% CI, 72-83] ms and 73 [95% CI, 67-81] ms; n.s.) and increased in the propofol group (80 [95% CI, 74-86] ms and 92 [95% CI, 84-102] ms; P=0.02). E(a) decreased in the propofol group only (18.8 [95% CI, 16.5-19.9] cm s(-1) and 16.0 [95% CI, 14.9-17.9] cm s(-1); P=0.003). From step 2a to step 2b, IVRT(c) increased further in the propofol group (109 [95% CI, 99-121] ms and 119 [95% CI, 99-135] ms; P=0.04) but remained stable in the other two groups. E(a) did not change from step 2a to step 2b. CONCLUSIONS: Halothane and sevoflurane did not impair LV relaxation, whereas propofol caused a mild impairment. However, the impairment by propofol was of a magnitude that is unlikely to cause clinical diastolic dysfunction.

Adolescent↗
PubMed2005

The suppression of spinal F-waves by propofol does not predict immobility to painful stimuli in humans.

BACKGROUND: The immobilizing effects of volatile anaesthetics are primarily mediated at the spinal level. A suppression of recurrent spinal responses (F-waves), which reflect spinal excitability, has been shown for propofol. We have assessed the concentration-dependent F-wave suppression by propofol and related it to the logistic regression curve for suppression of movement to noxious stimuli and the effect on the bispectral index (BIS). The predictive power of drug effects on F-waves and BIS for movement responses to noxious stimuli was tested. METHODS: In 24 patients anaesthesia was induced and maintained with propofol infused by a target controlled infusion pump at stepwise increasing and decreasing plasma concentrations between 0.5 and 4.5 mg litre(-1). The F-waves of the abductor hallucis muscle were recorded at a frequency of 0.2 Hz. BIS values were recorded continuously. Calculated propofol concentrations and F-wave amplitude and persistence were analyzed in terms of a pharmacokinetic-pharmacodynamic (PK/PD) model with a simple sigmoid concentration-response function. Motor responses to tetanic electrical stimulation (50 Hz, 60 mA, 5 s, volar forearm) were tested and the EC(50tetanus) was calculated using logistic regression. RESULTS: For slowly increasing propofol concentrations, computer fits of the PK/PD model for the suppression by propofol yielded a median EC50 of 1.26 (0.4-2.3) and 1.9 (1.0-2.8) mg litre(-1) for the F-wave amplitude and persistence, respectively. These values are far lower than the calculated EC(50) for noxious electrical stimulation of 3.75 mg litre(-1). This difference results in a poor prediction probability of movement to noxious stimuli of 0.59 for the F-wave amplitude. CONCLUSIONS: F-waves are almost completely suppressed at subclinical propofol concentrations and they are therefore not suitable for prediction of motor responses to noxious stimuli under propofol mono-anaesthesia.

Adult↗
PubMed2000

Propofol decreases stimulated dopamine release in the rat nucleus accumbens by a mechanism independent of dopamine D2, GABAA and NMDA receptors.

Although propofol (2,6-di-isopropylphenol) is a popular i.v. general anaesthetic, it has been suggested to have abuse potential. As many drugs of abuse act preferentially via release of dopamine in the limbic system, we investigated the action of propofol on stimulated dopamine release in the rat nucleus accumbens. Nucleus accumbens slices were superfused (1.6 ml min-1) with artificial cerebrospinal fluid at 32 degrees C. Dopamine release was evoked by electrical stimulation (10 pulses, 0.1 ms, 10 mA, 10 Hz, every 10 min) and monitored by fast cyclic voltammetry. Propofol 100 mumol litre-1 reduced stimulated dopamine release over the 2 h after administration, relative to intralipid controls, to mean 30 (SEM 2)% (P < 0.01). The dopamine D2 receptor antagonist metoclopramide 0.3 mumol litre-1 increased dopamine release but did not block the effect of propofol (38 (3)%). The selective GABAA antagonist bicuculline 24 mumol litre-1 also failed to antagonize the action of propofol (45 (3)%). The NMDA receptor antagonist dextromethorphan 10 mumol litre-1 decreased dopamine release to 57 (6)% (P < 0.01) but failed to block the inhibitory effect of propofol (46 (6)%). Although propofol has been reported to bind to D2, GABAA and NMDA receptors, failure of metoclopramide and bicuculline to block its effects suggests that an agonist action at D2 or GABAA receptors does not mediate the effects of propofol on dopamine release in the rat nucleus accumbens. The lack of effect of dextromethorphan makes an NMDA receptor antagonist action unlikely.

Anesthetics, Intravenous↗
PubMed2001

Propofol action in both spinal cord and brain blunts electroencephalographic responses to noxious stimulation in goats.

STUDY OBJECTIVES: Anesthetics, including propofol, depress the electroencephalogram (EEG) and neuronal activity in the midbrain reticular formation (MRF). Because propofol has anesthetic effects in the spinal cord, we hypothesized that it would indirectly depress EEG and MRF neuronal responses to noxious stimulation in part by a spinal cord action. DESIGN: Six goats were anesthetized with isoflurane and the jugular veins and carotid arteries were isolated to permit cranial bypass and differential propofol delivery. A noxious mechanical stimulus was applied to the distal forelimb while recording bifrontal EEG and MRF single-unit activities. Propofol was separately administered to the cranial (0.08 +/- 0.06 mg/kg) and torso circulations (4 mg/kg) and the noxious stimulus applied at 1,5, 10, and 15 min after each injection. SETTING: N/A. PATIENTS OR PARTICIPANTS: N/A. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Noxious stimulation decreased total power (TP) from 96 +/- 33, microV2/Hz to 38 +/- 20microV2/Hz, (mean +/- SD) and increased spectral edge frequency (SEF) from 10 +/- 3 Hz to 19 +/- 5 Hz (p<0.01). Propofol administered to the torso prevented stimulus-evoked changes in TP (121+/- 80 microV2/Hz, 121 +/- 74 microV2/Hz, 114 +/- 74 microV2/Hz at 1,5, and 10 min respectively, p<0.01 compared to control evoked response) and SEF (11 +/- 6Hz, 9 +/- 2Hz, 10 +/- 6Hz, and 12 +/- 5Hz at 1, 5, 10 and 15 min, respectively, p<0.001 compared to control evoked response). Propofol administered to the cranial circulation significantly blunted the EEG and MRF response, while torso-administered propofol had slight effects on MRF responses. CONCLUSIONS: Propofol blunted the EEG response to noxious stimulation in part via a subcortical action.

Analgesics↗
PubMed1995

The influence of propofol on vomiting induced by apomorphine.

It has been proposed that propofol has antiemetic effects even in nonsedative doses. The aim of this study was to investigate whether propofol influences vomiting induced by the dopamine agonist apomorphine. Ten healthy male volunteers received apomorphine infusion (1 mg/min) until vomiting was induced on four different occasions in a randomized order: a) during propofol infusion (2.4 +/- 0.7 mg.kg-1.h-1, mean +/- SD) at a sedation score of Grade 2-3 on a 5-grade scale; b) during midazolam infusion (0.13 +/- 0.04 mg.kg-1.h-1) at a sedation score of Grade 2-3 on a 5-grade scale; c) after a single nonsedating bolus dose propofol 0.4 mg/kg; and d) during infusion of normal saline. The amount of apomorphine needed to induce vomiting was increased after sedation with propofol (P = 0.005) as well as midazolam (P = 0.001). There was no difference in the sensitivity to apomorphine between these sedative regimens. The nonsedating single bolus propofol did not change the sensitivity to apomorphine compared to the saline infusion. We conclude that propofol given in a nonsedative dose has no effect on apomorphine-induced vomiting. However, the total amount of apomorphine given to induce vomiting was significantly larger during propofol sedation than during saline infusion. This was probably an effect of sedation inasmuch as a similar result was achieved during midazolam sedation.

Adult↗
PubMed1996

Spectral analysis of arterial pressure variability during induction of propofol anesthesia.

We studied the effect of continuous infusion of propofol on spectral components in systemic arterial pressure (SAP) signals in 35 consenting patients undergoing abdominal surgery. Anesthesia was induced with intravenous bolus administration of propofol (2.0 mg/kg), followed by infusion at either 5 mg.kg-1.h-1 (Group 1, n = 18) or 10 mg.kg-1.h-1 (Group 2, n = 17). Tracheal intubation was facilitated by administration of vecuronium (0.1 mg/kg). The SAP signal was subjected to off-line spectral analysis to obtain changes in power of the very low frequency (VLF; 0.00-0.08 Hz), low frequency (LF; 0.08-0.15 Hz), high frequency (0.15-0.25 Hz); and very high frequency (VHF; 0.80-1.60 Hz) components. Venous blood for the measurement of plasma concentration of propofol was collected at 5 min before bolus injection of propofol; at 5, 10, and 15 min after infusion of propofol; and immediately after endotracheal intubation. Infusion of propofol significantly decreased the total power of SAP spectrum in both groups, especially the VLF, LF, and VHF components at all intervals except postintubation. Immediately after tracheal intubation, patients in Group 1 showed a significant increase in mean arterial pressure when compared with those in Group 2 (118 +/- 5 mm Hg vs 102 +/- 5 mm Hg, P < 0.05). Similar change was also seen in the VLF component (7.4 +/- 0.7 mm Hg2 vs 4.4 +/- 0.5 mm Hg2, P < 0.05). After tracheal intubation, patients in Group 1 showed 15.7-, 3.3-, and 4.4-fold increase in the VLF, LF, and VHF components, respectively. There were 14.1-, 2.8-, and 2.8-fold increases in the respective components of the SAP signal in Group 2. At all intervals, the spectral components of SAP, however, did not correlate well with the plasma concentration of propofol in either group. These results suggest that spectral analysis of SAP signals may provide an alternative for assessing autonomic activities, such as the sympathetic response, to tracheal intubation during propofol anesthesia.

Abdomen↗