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PubMed1999

High dose propofol enhances red cell antioxidant capacity during CPB in humans.

PURPOSE: To compare low vs. high dose propofol and isoflurane on red cell RBC antioxidant capacity in patients during aortocoronary bypass surgery (ACBP). METHODS: Twenty-one patients, for ACBP, were anesthetized with sufentanil 0.5-10 microg x kg(-1) and isoflurane 0-2%; ISO = control; n = 7), or sufentanil 0.3 microg x kg(-1), propofol 1-2.5 mg x kg(-1) bolus then 100 microg x kg(-1) min(-1) before, and 50 microg x kg(-1) x min(-1) during CPB (LO; n = 7), or sufentanil 0.3 microg x kg(-1), propofol 2-2.5 mg x kg(-1) bolus then 200 microg x kg(-1) x min(-1) (HI; n = 7). Venous blood was drawn pre- and post-induction, after 30 min CPB, 5, 10, and 30 min of reperfusion, and 120 min post-CPB to measure red cell antioxidant capacity (malondialdehyde (MDA) production in response to oxidative challenge with t-butyl hydrogen peroxide) and plasma propofol concentration. Pre- induction blood samples were analyzed for antioxidant effects of nitrates on red cells. The tBHP concentration response curves for RBC MDA in ISO, LO and HI were determined. RESULTS: Preoperative nitrate therapy did not effect RBC MDA production. Perioperative RBC MDA production was similar in ISO and LO groups. Sustained intraoperative decrease in RBC MDA was seen with propofol 8.0+/-2.4 - 11.8+/-4.5 microg x ml(-1) in HI (P<0.05-0.0001). MDA production vs. log plasma propofol concentration was linear in HI dose. CONCLUSIONS: During CPB, RBC antioxidant capacity is enhanced and maintained with HI dose propofol. Propofol, at this dose, may prove useful in protecting against cardiopulmonary ischemia-reperfusion injury associated with ACBP.

Adult↗
PubMedDate not supplied

Nitrous oxide produces minimal hemodynamic changes in patients receiving a propofol-based anesthetic: an esophageal Doppler ultrasound study.

PURPOSE: Nitrous oxide (N(2)O) is a frequently used adjunct to propofol anesthesia. Although N(2)O reduces the requirement of propofol for induction and maintenance, the effects of both drugs on overall hemodynamics remain controversial. We tested the hypothesis that the addition of N(2)O to therapeutic doses of propofol alters hemodynamics and Doppler-derived variables evaluated with the esophageal Doppler monitor in a randomized, double-blinded, placebo-controlled design. METHODS: Thirty ASA I-II patients (aged 30-66 yr) were randomly assigned to receive propofol with oxygen-enriched air (FIO(2) = 0.3; air group) or propofol with 70% N(2)O (N(2)O group). Following intubation, a computerized target-controlled infusion technique was used to administer propofol from 0 micro g x mL(-1) (baseline) to 5 micro g x mL(-1) in 1 micro g x mL(-1) increments. RESULTS: Mean arterial pressure (MAP) decreased more in the N(2)O group than in the air group only at 5 micro g x mL(-1). Aortic blood flow (ABF) showed a similar dose-dependent decrease in both groups. Peak aortic flow acceleration, as a myocardial contractility index, decreased significantly and similarly in both groups in a dose-dependent manner whereas peak velocity of ABF, as another measure of myocardial contractility, remained unchanged. Heart rate-corrected left ventricular ejection time, as a measure of preload, remained constant in both groups at any target plasma concentration. CONCLUSION: Propofol causes dose-dependent decreases in ABF and MAP; however, 70% N(2)O produces minimal hemodynamic and Doppler-derived variable changes under target-controlled propofol infusion at therapeutic concentrations.

Adult↗
PubMed2000

Interaction of nitrous oxide and propofol to reduce hypertensive response to stimulation.

PURPOSE: To evaluate the interaction between nitrous oxide and propofol for the suppression of hypertension following electrical stimulation of the mental nerve in the rabbit. METHODS: Male Japan White rabbits were tracheostomized, cannulated and mechanically ventilated under isoflurane anesthesia. Square wave pulses (5 V, 0.5 msec, 50 Hz for 5 sec) were delivered to the left mental nerve. Animals received nitrous oxide 20, 40, 60 and 80% (Group 1); propofol 200, 400, 600 and 800 microg x kg(-1) min(-1) (Group 2); or combinations of nitrous oxide and propofol at 10 + 100, 20 + 200, 30 + 300 and 40 % + 400 microg x kg(-1) x min(-1) (Group 3). Systolic blood pressure was recorded from immediately before to maximal increase following nerve stimulation. Probit analysis was used to obtain ED(50) values for 50% suppression of blood pressure elevation. Isobolographic analysis was used to evaluate the interaction between nitrous oxide and propofol. RESULTS: ED(50) values are 52.9% for nitrous oxide (Group 1), 464.1 microg x kg(-1) min(-1) for propofol (Group 2), 21.7 % + 217.1 microg x kg(-1) min(-1) for nitrous oxide and propofol combination (Group 3) and 24. 7 % + 247.1 microg x kg(-1) x min(-1) for the theoretically additive combination of nitrous oxide and propofol, respectively. CONCLUSION: The interaction between nitrous oxide and propofol for the suppression of blood pressure elevation following electrical stimulation of the mental nerve is additive.

Anesthetics, Inhalation↗
PubMed2000

Effects of propofol containing EDTA on mineral metabolism in medical ICU patients with pulmonary dysfunction.

OBJECTIVE: To determine whether the addition of disodium edetate (EDTA) to propofol significantly alters mineral metabolism, adverse events, and outcome in critically ill medical patients with acute pulmonary dysfunction. DESIGN: Multicentre, double-randomised, double-blind, comparative trial. SETTING: Medical intensive care units of 5 health centres. PATIENTS: A total of 85 haemodynamically stable men and women aged 18-81 years who had pulmonary dysfunction or adult respiratory distress syndrome as a primary diagnosis or complication and who were expected to require at least 48 hours of sedation and mechanical ventilation. INTERVENTIONS: Patients were randomised to receive propofol with or without EDTA and then to 1 of 2 sedation levels: light (Modified Ramsay Sedation Scale [MRSS] score of 2 to 3) or deep (MRSS score of 4 to 5). Propofol was administered by continuous infusion at an initial rate of 5 microg/kg per min and titrated as needed. MEASUREMENTS AND RESULTS: Approximately 63 % of patients had a high severity of illness as indicated by an Acute Physiology and Chronic Health Evaluation II score > or = 19. As expected, these patients had a higher mortality rate but did not require a higher dose of propofol or propofol with EDTA. Extensive evaluation of cation homeostasis showed that ionised calcium and magnesium concentrations remained remarkably stable during treatment. Total calcium concentration was low as a result of hypoalbuminemia. Parathyroid hormone (PTH) concentration was elevated in both study groups at baseline, on day 4, and at the end of sedation. There were no significant differences in electrolyte levels and no progression to renal dysfunction. There were also no significant differences in haemodynamic or adverse-event profiles. Treatment-related adverse events occurred in 5 patients in each group; 4 of these (in 3 patients receiving propofol and 1 patient receiving propofol with EDTA) were considered serious. Because a large percentage of patients experienced a change in sedation level, no analyses were performed using sedation level. CONCLUSIONS: The addition of EDTA to propofol does not alter calcium and magnesium homeostasis in critically ill patients with acute pulmonary dysfunction. The reason for the elevation in PTH concentrations in such patients is not known.

Adult↗
PubMed2006

Protective effects of propofol on lipopolysaccharide-activated endothelial cell barrier dysfunction.

BACKGROUND: Propofol has been widely used in intravenous anesthesia. It possesses antioxidant and immunomodulating effects. This study aimed to investigate whether propofol may attenuate lipopolysaccharide (LPS)-induced endothelial cell barrier dysfunction and the possible mechanisms of such modulation. METHODS: Cultured human umbilical vein endothelial cells (HUVECs) were used to assess the following treatments: (i) no additives (negative control), (ii) LPS alone (1 and 10 microg/ml), (iii) propofol alone (20 microg/ml), (iv) intralipid (a solvent of propofol) alone (20 microg/ml), (v) LPS (10 microg/ml) combination with propofol (4 and 20 microg/ml) and (vi) LPS (10 microg/ml) combination with intralipid (20 microg/ml). Changes of cell permeability and filamentous actin (F-actin) were determined. Expression of nitrotyrosine proteins and activity of nuclear factor kappaB (NF-kappaB) were analyzed by Western blot and immunocytochemistry. Expression of endothelial nitric-oxide synthase (eNOS) and inducible nitric-oxide synthase (iNOS) were analyzed by reverse transcriptase-polymerase chain reaction. RESULTS: LPS markedly increased the permeability of endothelial cells, the formation of peroxynitrite and depolymerization of F-actin in HUVECs. LPS also significantly increased mRNA of iNOS, protein level of NF-kappaB and decreased mRNA of eNOS (P < 0.05). Propofol at both concentrations (4 and 20 microg/ml) significantly inhibited the LPS-induced increase in cell permeability and alteration in F-actin organization. Propofol also reduced the LPS-enhanced iNOS mRNA and NF-kappaB protein levels whilst it increased eNOS mRNA expression (P < 0.05). CONCLUSION: This study demonstrated that propofol, both at therapeutic concentrations and 5 times therapeutic concentrations, inhibited NF-kappaB activation in LPS-stimulated endothelial cells and was found to protect endothelial cells against LPS-induced barrier dysfunction.

Actins↗
PubMed2006

[Pharmacodynamics of two different propofol formulations].

BACKGROUND: Propofol is nowadays available in various lipid formulations. We compared two different propofol formulations with respect to pharmacodynamics, using the EEG and clinical signs. MATERIALS AND METHODS: Ten volunteers received Diprivan 1% and Propofol 1% MCT Fresenius as a computer controlled infusion with increasing propofol target concentrations. A sigmoid E(max) model with effect compartment was estimated for the median frequency of the EEG power spectrum, based on measured arterial propofol plasma concentrations. Clinical pharmacodynamics were assessed by reaction on acoustic stimuli, eyelid reflex and corneal reflex. RESULTS: The drugs did not differ in pharmacodynamics with respect to EEG (EC(50) 2.1+/-0.6 for Diprivan and 2.1+/-0.5 microg/ml for Propofol Fresenius) and clinical signs. The pharmacodynamic model was characterized by a steep concentration effect relationship and a distinct hysteresis between propofol plasma concentration and effect (k(e0) 0.12+/-0.04 and 0.12+/-0.5 min(-1)). CONCLUSIONS: The investigated lipid formulations have no influence on the pharmacodynamics of propofol.

Acoustic Stimulation↗
PubMed1996

[Neuromuscular blockade after atracurium and alcuronium with propofol and thiopental].

UNLABELLED: Does propofol or thiopentone enhance the effect of nondepolarizing muscle relaxants? We evaluated the effects of propofol and thiopentone on the pharmacodynamics of atracurium and alcuronium in 43 surgical patients (ASA I and II) under general anaesthesia. METHODS: The patients were randomized into five groups, A-E. Anaesthesia was induced in all patients with fentanyl 4 micrograms/kg i.v. Patients in groups A and C patients received thiopentone 7 mg/kg i.v., and relaxation was achieved with alcuronium 0.25 mg/kg (group A) and atracurium 0.5 mg/kg (group C). Electromyography (train of four, TOF) was used to determine the time of onset of relaxation (AZ) and the maximum degree of blockade (T%). The recovery times to 25%, 50% and 75% of baseline muscle strength were recorded. Additionally, the TOF ratio T4:T1 was calculated, indicating the probable end of relaxation at a ratio of 0.7. At the beginning of the recovery phase (T1 = 15%) propofol 1% 3 mg/kg was given, and the effect on the TOF was measured. Patients in groups B and D patients received total intravenous anaesthesia (TIVA) with propofol 1% 6-12 mg/kg per hour continuously after induction with 3 mg/kg. The action profile of alcuronium 0.25 mg/kg (group B) and atracurium 0.5 mg/kg (group D) were recorded. Group E patients received thiopentone (10 mg/kg per hour) under the use of atracurium 0.5 mg/kg. Ventilation was performed with 30%/70% oxygen and N2O. The results were analyzed for significance using the Mann-Whitney U-test (P = 0.019). RESULTS: A slight difference in AZ was noted for alcuronium under the use of TIVA between propofol and thiopentone: 13 min and 5 min, respectively. Otherwise, the pharmacodynamics (T% and recovery of neuromuscular function) of the two relaxants exhibited no major differences related to thiopentone, propofol or their combination. The TOF was not influenced under additional propofol application. Noteworthy were the wide distribution of the time course of action (up to 3 h) and the magnitude of T% depression under alcuronium. CONCLUSION: Propofol and thiopentone have no potentiating influence on the time course of action and the magnitude of relaxation with alcuronium and atracurium. Pharmacodynamics of nondepolarizing muscle relaxants do not seem to be influenced by these two hypnotics.

Adjuvants, Anesthesia↗
PubMed1997

[Propofol and postoperative nausea and/or vomiting].

UNLABELLED: The objective of this prospective, randomised study was to investigate the incidence of postoperative nausea and/or vomiting (PONV) during the first 24 h postoperatively. For a quality assurance study on PONV, we compared two established general anaesthetic procedures in 239 patients undergoing four different types of surgery (subtotal thyroidectomy, laparotomy for gynaecological procedures, laparoscopy, and surgery for extra-abdominal procedures). METHODS: All eligible patients provided informed consent. For premedication temazepam 10-20 mg was administered orally. We used propofol (1.5-2 mg/kg) for induction of anaesthesia in all patients, followed by 0.1-0.3 mg fentanyl, 2.5-5 mg droperidol, and for muscular relaxation atracurium or pancuronium according to body weight. Maintenance of general anaesthesia in group A was by administration of isoflurane in a maximum concentration of 0.6 vol.% in 70% nitrous oxide and 30% oxygen and in group B by continuous infusion of propofol (5-8 mg/kg.h) and normoventilation with oxygen in air (Fi02 = 0.3). In both groups additional analgesia was provided intraoperatively by equal dosages of fentanyl up to a maximum of 0.6 mg and clonidine up to 200 micrograms. Episodes of PONV were registered following extubation, during the first 4 h postoperatively, during the period 4-24 h postoperatively, and after the first mobilisation. Pain scores were recorded with the aid of a visual analogues scale. The statistical evaluation was performed using the chi-square or Wilcoxon test. RESULTS AND DISCUSSION: In patients undergoing thyroidectomy or laparotomy, continuous infusion of propofol drastically reduced the incidence of PONV in the first 24 h postoperatively, particularly during the first 4 h (25/41 vs 10/41, resp. 20/32 vs 11/31). The overall incidence of PONV was higher in the first half of the menstrual cycles decreased with patient age, increased with the duration of anaesthesia, and was higher in patients with a history of motion sickness. With the same level of analgesia in both groups, the differences disappeared in the further postoperative course. The use of similar dosages of opioids for pain control in these groups might explain this observation. PONV occurred extremely rarely in patients undergoing laparoscopy (1 resp. 2 of 34), and in those undergoing surgery for extra-abdominal procedures did not occur at all. The explanation may be that the induction of anaesthesia with propofol was followed only by a relatively short duration of general anaesthesia for these surgical procedures, and postoperative pain control was performed solely with non-opioids. CONCLUSIONS: We found that the antiemetic effect of propofol was considerable in the early postoperative period. The higher cost of propofol as compared to other induction agents can be covered by not using nitrous oxide for maintenance of anaesthesia and by the decreased need for antiemetic drugs postoperatively. According to the calculations of our clinical pharmacy, the costs of the propofol infusion regimen exceeded those of balanced anaesthesia by 8.50 DM/h; the need for antiemetics was one-half that of the non-propofol group. Considering a cost of 16 DM for cleaning the bed after vomiting, improvement of the patient's condition during the postoperative period can be achieved without additional expense.

Adult↗
PubMed1998

[Remifentanil-propofol anesthesia in vertebral disc operations: a comparison with desflurane-N2O inhalation anesthesia. Effect on hemodynamics and recovery].

OBJECTIVE: To ascertain whether there is a difference between total intravenous anaesthesia with propofol (P) and remifentanil (R) and inhalational anaesthesia with desflurane (D) and nitrous oxide (N) with regard to haemodynamic reactions, recovery profile and postoperative analgesic demand in patients scheduled for elective microsurgical vertebral disc resection. METHODS: 50 patients (ASA I-II, 18-65 years) were randomly assigned to receive total intravenous anaesthesia with propofol and remifentanil or inhalational anaesthesia with desflurane and nitrous oxide. After standardised induction of anaesthesia in both groups (1 microgram.kg-1 remifentanil, 1.5 mg.kg-1 propofol 0.1 mg.kg-1 cisatracurium), anaesthesia was maintained in the D/N group with desflurane in 50% N2O. The patients of the P/R group received a constant infusion of 2 mg.kg-1.h-1 propofol and a constant infusion of 0.5 microgram.kg-1.min-1 remifentanil, which was reduced after 15 min by 50%. The administration of desflurane and the infusion of the anaesthetics were adjusted to maintain a surgical depth of anaesthesia. At the end of surgery the anaesthetics were discontinued and early emergence from anaesthesia was assessed by measuring time to spontaneous ventilation (VT > 4 ml/kg), tracheal extubation, opening of the eyes and stating correct name and data of birth. The frequency of analgesics and total demand for analgesics were determined using patient-controlled analgesia and recorded for 2 h postoperatively. In addition the pain level of the patients was measured on a visual analogue scale and the incidence of postoperative shivering, nausea and vomiting was noted. RESULTS: Patients anaesthetised with desflurane responded to tracheal intubation and skin incision with increasing blood pressure and showed higher heart rates than patients anaesthetised with propofol and remifentanil, but there were no other haemodynamic differences between the groups in response to surgical stimuli. There were significantly shorter times to spontaneous ventilation (3.2 vs. 6.3 min), extubation (3.8 vs. 9.5 min), eye opening (3.0 vs. 11.5 min) and giving name and date of birth (4.8 vs. 14.3 min) in patients anaesthetised with remifentanil and propofol than in those receiving desflurane and nitrous oxide. In addition, patients anaesthetised with remifentanil and propofol had a greater incidence of postoperative shivering. There were no significant differences between the two groups in the patients' pain scores, analgesic demand and incidence of nausea and vomiting. CONCLUSION: Patients anaesthetised with propofol and remifentanil have significantly shorter emergence times than patients anaesthetised with desflurane and nitrous oxide. The low incidence of postoperative pain after microsurgical vertebral disc resections requires no large-scale analgesic therapy, even after total intravenous anaesthesia including remifentanil.

Adult↗
PubMed2003

The pathophysiology of propofol infusion syndrome: a simple name for a complex syndrome.

Propofol infusion syndrome (PRIS) is a rare and often fatal syndrome described in critically ill children undergoing long-term propofol infusion at high doses. Recently several cases have been reported in adults, too. The main features of the syndrome consist of cardiac failure, rhabdomyolysis, severe metabolic acidosis and renal failure. To date 21 paediatric cases and 14 adult cases have been described. These latter were mostly patients with acute neurological illnesses or acute inflammatory diseases complicated by severe infections or even sepsis, and receiving catecholamines and/or steroids in addition to propofol. Central nervous system activation with production of catecholamines and glucocorticoids, and systemic inflammation with cytokine production are priming factors for cardiac and peripheral muscle dysfunction. High-dose propofol, but also supportive treatments with catecholamines and corticosteroids, act as triggering factors. At the subcellular level, propofol impairs free fatty acid utilisation and mitochondrial activity. Imbalance between energy demand and utilisation is a key pathogenetic mechanism, which may lead to cardiac and peripheral muscle necrosis. Propofol infusion syndrome is multifactorial, and propofol, particularly when combined with catecholamines and/or steroids, acts as a triggering factor. The syndrome can be lethal and we suggest caution when using prolonged (>48 h) propofol sedation at doses higher than 5 mg/kg per h, particularly in patients with acute neurological or inflammatory illnesses. In these cases, alternative sedative agents should be considered. If unsuitable, strict monitoring of signs of myocytolysis is advisable.

Adult↗
PubMed2004

Premedication medicines do not cause drug metabolic interaction with propofol using human liver microsomes in vitro.

OBJECTIVE: Propofol (2,6-diisopropylphenol) is widely used for anesthetic induction as well as for chronic sedation in intensive care units. In this study, we investigated the interaction between propofol and premedications, i.e., psychotropic and antianxiety agents (diazepam, midazolam), hypnotics (thiamylal), local anesthetics (lidocaine), depolarizing muscular relaxants (vecuronium), an antihypertensive (clonidine) and an H2-receptor antagonist (cimetidine) using human liver microsomes in vitro. METHODS: The interaction effects between propofol and premedications were examined using human liver microsomal preparation in vitro. The concentration of propofol was determined by HPLC with UV detection. RESULTS: The apparent Michaelis-Menten constant (Km) and the maximal velocity of total metabolic formation (Vmax) of propofol in human liver microsomes were 123 microM and 26.1 micromol/min per milligram of mg protein, respectively. Seven premedications (diazepam, midazolam, thiamylal, lidocaine, cimetidine, vecuronium, and clonidine) did not inhibit propofol metabolism in human liver microsomes at concentrations within the therapeutic range. CONCLUSIONS: These results showed no interactions between propofol and seven premedication drugs within the therapeutic range of propofol using human liver microsomes in vitro.

Anesthetics, Intravenous↗
PubMed2006

Prediction of total propofol clearance based on enzyme activities in microsomes from human kidney and liver.

OBJECTIVE: Propofol is commonly used for anesthesia and sedation in intensive care units. Approximately 53% of injected propofol is excreted in the urine as the glucuronide and 38% as hydroxylated metabolites. Liver, kidneys and intestine are suspected as clearance tissues. We investigated the contribution of the liver and kidneys to propofol metabolism in humans using an in vitro-in vivo scale up approach. METHODS: Renal tissue was obtained from five patients who received nephrectomies. Each renal hydroxylation and glucuronidation enzymatic activities in microsomal fractions from patients were performed discretely and their estimation based on the decrease of propofol concentration. Hepatic hydroxylation and glucuronidation activities were also performed separately using human liver microsomes. This estimation is based on the decrease of propofol concentration, assuming that the contribution of hydroxylation activity without NADPH-generating system and glucuronidation activity without UDPGA in each microsomal fraction are negligible. Both renal and hepatic clearances were estimated assuming a well-stirred model. RESULTS: Enzymatic activity of propofol oxidation in renal microsomes was negligible. Although glucuronidation activity in microsomes from kidneys was comparable to that from liver, the hepatic intrinsic clearance predicted from in vitro study was higher than that in kidneys due to the larger tissue volume and higher protein concentration. However, glucuronidation clearance in kidney is relatively similar to that in liver because of blood flow limitation of clearance in both tissues. CONCLUSION: The high degree of hydroxylation activity in liver microsomes is consistent with the blood flow-limited hepatic clearance of propofol. Although the activity of propofol glucuronidation in liver is higher, glucuronidation in kidney may be a substantial contributor.

Aged↗
PubMed2001

Death after excessive propofol abuse.

Abuse of the anaesthetic agent propofol (2,6-diisopropylphenol) is rare, but we report a case of a 26-year-old male nurse in which the autopsy showed unspecific signs of intoxication and criminological evidence pointed towards propofol abuse and/or overdose. Intravenously administered propofol is a fast and short-acting narcotic agent, therefore it seemed questionable whether the deceased would have been able to self-administer a lethal overdose before losing consciousness. The blood and brain concentrations corresponded to those found 1-2 min after bolus administration of a narcotic standard dose of 2.5 mg propofol/kg body weight. Extremely high propofol concentrations were found in the urine indicating excessive abuse before death. However, due to the short half-life of propofol, the cumulative effects of repeated injections should not be relevant for toxicity, since this would result in a blood level increase of only 1-2 micrograms/ml. Furthermore, the detection and quantitation of propofol in three different hair segments indicated chronic propofol abuse by the deceased. The results of the investigation suggest that death was not caused by a propofol overdose but by respiratory depression resulting from overly rapid injection.

Adult↗
PubMed2004

The effects of isoflurane and propofol on intraoperative neurophysiological monitoring during spinal surgery.

OBJECTIVES: To compare the effects of isoflurane and propofol on intraoperative neurophysiological monitoring (IONM) during spinal surgery. METHODS: Thirty-five patients were randomly assigned to receive isoflurane (n = 17) or propofol (n = 18) anesthesia. Somatosensory evoked potentials (SEPs) following posterior tibial nerve stimulation were recorded before induction as baselines. Isoflurane concentrations and propofol infusions were adjusted to obtain four pre-determined BIS ranges: 65-55, 55-45, 45-35 and 35-25. For each range, a stable state was maintained for at least 10 min to perform IONM. The SEP latency P40 and amplitude P40-N50, the onset latency and amplitude of transcranial motor evoked potentials (tcMEPs), and threshold intensity of triggered electromyographic activity (EMG) following pedicle screw stimulation were statistically analyzed. RESULTS: Compared with baseline values, P40 latency increased and P40-N50 amplitude decreased after anesthesia with isoflurane or propofol. Isoflurane caused a dose-dependent depression of SEPs, but propofol did not. TcMEPs were recordable and stable in all patients receiving propofol in each BIS range, but only recordable in 10 (58.8%) receiving isoflurane with BIS >55, and 3 (17.8%) with BIS <55. No difference was noted in triggered EMG. CONCLUSIONS: Isoflurane inhibited IONM more than propofol. Propofol is recommended for critical spinal surgery, particularly when motor pathway function is monitored.

Adolescent↗
PubMed2006

The influence of sevoflurane on the bispectral index, regional cerebral oxygen saturation, and propofol concentration during propofol/N2O anesthesia.

OBJECTIVE: This study was undertaken to investigate the influence of sevoflurane on the bispectral index (BIS), regional cerebral oxygen saturation (rSO(2)), and serum propofol concentration during propofol/N(2)O anesthesia. This study tested the hypothesis that sevoflurane affect BIS values, rSO(2), and the pharmacokinetics of propofol during propofol/ N(2)O anesthesia. METHODS: General anesthesia was administered to 15 ASA I-II patients with a continuous infusion of propofol to maintain a BIS value of 45 +/- 5. After recording baseline values, patients were assigned to receive sevoflurane (2.0%, 20 min). BIS values, rSO(2) using near-infrared spectroscopy, and hemodynamic parameters were recorded for 60 min. Cardiac output (CO) and stroke volume (SV) were evaluated using impedance cardiograph methods. Propofol concentration was determined using high-performance liquid chromatography. RESULTS: Sevoflurane (2.0%, 20 min) decreased the BIS score from 47.4 +/- 8.2 to 27.3 +/- 5.9 (P < 0.01, n = 15) without affecting rSO(2). Sevoflurane decreased systolic blood pressure from 112.1 +/- 14.0 mmHg to 96.5 +/- 13.2 mmHg (P < 0.001, n = 15) without affecting heart rate. Both CO and SV were significantly decreased during sevoflurane application. Propofol concentration was increased from 2.71 +/- 0.51 microg/ml to 3.30 +/- 0.57 microg/ml (P < 0.05) after sevoflurane application, and was returned to baseline after sevoflurane washout. CONCLUSIONS: We have shown that sevoflurane decreases BIS values during propofol/N(2)O anesthesia without affecting rSO(2) and that this change is accompanied by an increase in serum propofol concentration. Changes in propofol concentration may be due to, at least in part, hemodynamic changes such as decreased CO produced by sevoflurane.

Adult↗
PubMed1992

Inhibition of lipid peroxidation in isolated rat liver mitochondria by the general anaesthetic propofol.

The effect of the general anaesthetic propofol (2,6-diisopropylphenol) on lipid peroxidation in rat liver mitochondria was assessed with the thiobarbituric acid (TBA) assay. Propofol was shown to inhibit the accumulation of TBA-reactive compounds after initiation of radical production by the addition of the ADP-Fe2+ complex. Analysis of kinetics showed that propofol caused a concentration-dependent delay as well as a decrease in the rate of the peroxidation process. 1H-NMR spectra of mitochondrial lipid extracts indicated that 95% of the added propofol remained intact after 30 min incubation under conditions of low oxidative stress. The ESR spectrum of propofol incubated in the presence of EDTA-Fe2+ and H2O2 as initiators of radical production showed a radical that was most likely a decomposition product of the primary phenoxy radical of propofol. It is concluded that (a) propofol acts as a chain reaction-breaking antioxidant by forming a stable radical and (b) propofol does not seem to be metabolized in mitochondria in vitro.

Adenosine Diphosphate↗
PubMed1991

Neurochemical action of the general anaesthetic propofol on the chloride ion channel coupled with GABAA receptors.

The effect of propofol, a novel short acting anaesthetic, on the function of the GABAA/ionophore receptor complex was studied in vitro in cortical membrane preparations from rat cerebral cortex and was compared with the action of pentobarbital and alphaxalone, two general anaesthetics known to enhance GABAergic transmission. Propofol, mimicking the action of pentobarbital and alphaxalone, increased [3H]GABA binding, reduced [35S]TBPS binding and enhanced muscimol-stimulated 36Cl- uptake in a concentration-dependent manner. While the efficacy of the drugs in affecting these biochemical parameters was similar, they differed markedly in potency being alphaxalone greater than propofol greater than pentobarbital. However, separate sites of action or different mechanisms for these drugs can be suggested by the result that the concomitant addition of propofol either with alphaxalone or pentobarbital or diazepam produced a simple additive inhibition of [35S]TBPS binding as well as an additive enhancement of [3H]GABA binding and muscimol-stimulated 36Cl- uptake. The effect of propofol at the level of the GABA/ionophore receptor complex seems to be strictly dependent on the interaction of GABA with its recognition site. In fact, the specific GABAA receptor antagonist bicuculline antagonized the decrease of [35S]TBPS binding as well as the enhancement of [3H]GABA binding and muscimol-stimulated 36Cl- uptake induced by propofol. On the other hand, propofol was able to enhance [3H]GABA binding in membranes previously incubated with the specific chloride channel blocker picrotoxin. Finally, the finding that propofol fails to affect [3H]flunitrazepam binding together with the failure of Ro 15-1788 and PK 11195 to antagonize its effect on [35S]TBPS binding excludes a direct interaction at the level of benzodiazepine recognition sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗
PubMed1996

[Effects of propofol on blood concentration of cyclosporine].

OBJECTIVE: This study was designed to assess whether propofol modifies the blood concentrations of cyclosporine and lipoproteins, which bind cyclosporine. STUDY DESIGN: Prospective open study. PATIENTS: Fifteen consecutive grafted patients, scheduled for surgery allowing them to resume their oral treatment postoperatively. Their immunosuppressive treatment, included cyclosporine (Cy A), at a steady-state dosage. METHODS: Blood samples were drawn and residual Cy A blood concentrations were measured the days before and after anaesthesia and before and immediately after discontinuing the propofol infusion. Serum triglycerides, cholesterol, high-density lipoprotein (HDL) concentrations were measured before and immediately after discontinuing the propofol infusion. RESULTS: The 15 patients were given propofol by infusion for 30-210 min (mean 85 +/- 59 min). They received a total dose of propofol of 696 +/- 497 mg, a total fentanyl dose of 175 +/- 82 micrograms, and a total midazolam dose of 2.8 +/- 0.8 mg. The residual cyclosporine blood concentrations were similar the day before (142 +/- 47 ng.mL-1) and following anaesthesia (128 +/- 46 ng.mL-1) (P = 0.08). Serum cholesterol concentrations were not significantly influenced by propofol infusion, but serum triglycerides levels increased (1.46 +/- 0.66 vs 1.97 +/- 0.81 g.L-1), and HDL and LDL levels decreased (0.54 +/- 0.20 vs 0.47 +/- 0.18 g.L-1; 1.44 +/- 0.42 vs 1.28 +/- 0.37 g.L-1). CONCLUSION: Propofol by infusion does not modify the cyclosporine concentration. It is concluded that propofol may be a suitable agent for intravenous anaesthesia in cyclosporine treated patients, provided a close postoperative monitoring of cyclosporine blood concentrations is maintained.

Adult↗