Differential effects of propofol, ketamine, and thiopental anaesthesia on the skeletal muscle microcirculation of normotensive and hypertensive rats in vivo

Background. This study utilized the dorsal microcirculatorychamber (DMC) model to determine differential effects of i.v.propofol, ketamine, and thiopental anaesthesia on the skeletalmuscle microcirculation (10–180 µm) of normotensive(Male Wistar Kyoto, WKY) and hypertensive (spontaneously hypertensiveHarlan, SHR) rats, importantly, comparing responses to a consciousbaseline. Methods. Three weeks following implantation of the DMC in WKY(n=8) and SHR (n=6) (130 g) 0.25 ml 100 g^–1 FITC–BSA(i.v.) was administered and the microcirculation viewed usingfluorescent in vivo microscopy for a 30 min baseline (t=0–30min). This was followed by either propofol, thiopental, ketamine,or saline (i.v. bolus induction over 5 min (t=30–35 min)),then maintenance step-up infusion for 60 min (t=45–105min), so that animals received all four agents 1 week apart(56 experiments). Results. Dilation of A3 arterioles (15–30 µm) andV3 venules (20–40 µm) with propofol was greaterin SHR (t=95 min, A3 36.7 (12)%, V3 15.5 (2.3)%) than WKY (t=95min, A3 19.4 (7.4)%, V3 8.0 (2.3)%) (P<0.05). Constrictionof A3 with ketamine was greater in SHR (t=95 min, A3 –29.1(6.4)%) than WKY (A3 –17.5 (8.8)%) (P<0.05). This wasaccompanied by hypotension with propofol in SHR (–32%decrease in systolic arterial pressure), but not WKY (–6%)and hypertension with ketamine in WKY (–15%) and SHR (–24%)(P<0.05). During thiopental anaesthesia there was dilationof A1 (80–180 µm), A3, and V3 in WKY (P<0.05).Conversely, in SHR dilation of venules (29.2 (8.7)%) was accompaniedby constriction of A1 and A3 (t=95 min, A1 –25.1 (5.9)%,A3 –45.2 (3.1)%) (P<0.05). Conclusion. Within the skeletal muscle microcirculation of hypertensiverats there is enhanced dilation with propofol and constrictionwith ketamine, associated with exaggerated changes in arterialpressure. Thus, dysfunctional control mechanisms at the levelof the microcirculation alter responses to anaesthesia duringhypertension.      

Intravenous anaesthesia and the rat microcirculation: the Dorsal Microcirculatory Chamber{dagger}

The use of the dorsal microcirculatory chamber in male Wistarrats (n=7) to study the effects of induction and maintenanceof anaesthesia on the microcirculation is described. Differentpatterns of responses were observed. At induction, arteriolardilation was found following propofol and thiopental but ketamineproduced constriction. During maintenance, constriction of arterioleswas seen with ketamine and thiopental but dilation persistedwith propofol. The dorsal microcirculatory chamber appears tobe a useful tool for the study of microcirculatory changes relatedto anaesthesia. Br J Anaesth 2000; 85: 901–3     

Propofol attenuates myocardial lipid peroxidation during coronary artery bypass grafting surgery

Background. Propofol can scavenge free radicals because it hasa chemical structure similar to antioxidants. Methods. We examined if free radical scavenging occurs withpropofol during CABG operations. We studied 24 patients undergoingCABG surgery for triple vessel disease, randomized into twogroups. After induction of anaesthesia with fentanyl 10 µgkg^–1 and midazolam 0.1 mg kg^–1, patients in thefentanyl group (n=14) received fentanyl infusion 10–30µg kg^–1 h^–1 and patients in the propofol group(n=10) received propofol infusion 3–6 mg kg^–1 h^–1for maintenance of anaesthesia. Atrial tissue biopsies weretaken during cannulation for bypass, 45 min after cross-clampinsertion, 5 min after unclamping, and in the decannulationperiod. Lipid peroxidation was assessed by measurement of thiobarbituricacid reactive substances (TBARS) in the atrial tissue samples. Results. Lipid peroxidation in the propofol group was less thanin the fentanyl group (P<0.05) in all sampling periods. Lipidperoxidation in the fentanyl group increased significantly duringcardiopulmonary bypass (CPB) (P<0.05), but no increase wasfound in the propofol group (P>0.05). Conclusion. In clinical doses, propofol strongly attenuateslipid peroxidation during CABG surgery. Br J Anaesth 2002; 89: 242–6     

Efficacy of prophylactic ketamine in preventing postoperative shivering

Background. Treatment with ketamine and pethidine is effectivein postoperative shivering. The aim of this study was to comparethe efficacy of low-dose prophylactic ketamine with that ofpethidine or placebo in preventing postoperative shivering. Methods. A prospective randomized double-blind study involved90 ASA I and II patients undergoing general anaesthesia. Patientswere randomly allocated to receive normal saline (Group S, n=30),pethidine 20 mg (Group P, n=30) or ketamine 0.5 mg kg^–1(Group K, n=30) intravenously 20 min before completion of surgery.The anaesthesia was induced with propofol 2 mg kg^–1, fentanyl1 µg kg^–1 and vecuronium 0.1 mg kg^–1. It wasmaintained with sevoflurane 2–4% and nitrous oxide 60%in oxygen. Tympanic temperature was measured immediately afterinduction of anaesthesia, 30 min after induction and beforeadministration of the study drug. An investigator, blinded tothe treatment group, graded postoperative shivering using afour-point scale and postoperative pain using a visual analoguescale (VAS) ranging between 0 and 10. Results. The three groups did not differ significantly regardingpatient characteristics. The number of patients shivering onarrival in the recovery room, and at 10 and 20 min after operationwere significantly less in Groups P and K than in Group S. Thetime to first analgesic requirement in Group S was shorter thanin either Group K or Group P (P<0.005). There was no differencebetween the three groups regarding VAS pain scores. Conclusion. Prophylactic low-dose ketamine was found to be effectivein preventing postoperative shivering.     

Propofol metabolism is enhanced after repetitive ketamine administration in rats: the role of cytochrome P-450 2B induction

Background. In a series of ex vivo and in vivo studies we investigatedthe ability of repetitive ketamine administration to alter themetabolism and anaesthetic effect of propofol and the role ofketamine-mediated P-450 2B induction in rats. Methods. Male Wistar rats were pretreated with 80 mg kg^–1ketamine i.p. twice daily for 4 days. Pentoxyresorufin O-dealkylation(PROD), P-450 2B protein and mRNA were determined. Residualpropofol concentration was measured after incubating hepaticmicrosomes with 100 µM propofol. Sleeping times inducedby i.p. 80 mg kg^–1 propofol were determined. Orphenadrine,a P-450 2B inhibitor, was added in both ex vivo and in vivostudies. Finally, serial whole blood propofol concentrationswere determined after i.v. infusion of 15 mg kg^–1 propofol. Results. Ketamine pretreatment produced 5.4-, 3.4- and 1.7-foldincreases in hepatic PROD activity, P-450 2B protein and mRNA,respectively. Residual propofol concentration was 46% lowerafter incubation with microsomes from ketamine-pretreated ratsthan in the control group. The addition of orphenadrine to ketamine-pretreatedmicrosomes produced an increase in residual propofol concentrationin a concentration-dependent manner. Ketamine pretreatment reducedpropofol sleeping time to 12% of the control, which was reversedby orphenadrine. The whole blood propofol concentration in ketamine-pretreatedrats was significantly lower than that of control rats at 1,2, 4 and 8 min after cessation of propofol infusion. Conclusions. Repetitive ketamine administration enhances propofolmetabolism and reduces propofol sleeping time in rats. We suggestthat P-450 2B induction may produce ketamine–propofolinteraction in anaesthetic practice.     

Measurement of motor evoked potentials following repetitive magnetic motor cortex stimulation during isoflurane or propofol anaesthesia

Background. Isoflurane and propofol reduce the recordabilityof compound muscle action potentials (CMAP) following singletranscranial magnetic stimulation of the motor cortex (sTCMS).Repetition of the magnetic stimulus (repetitive transcranialmagnetic stimulation, rTCMS) might allow the inhibition causedby anaesthesia with isoflurane or propofol to be overcome. Methods. We applied rTCMS (four stimuli; inter-stimulus intervalsof 3, 4, 5 ms (333, 250, 200 Hz), output 2.5 Tesla) in 27 patientsand recorded CMAP from the hypothenar and anterior tibial muscle.Anaesthesia was maintained with fentanyl 0.5–1 µgkg^–1 h^–1 and either isoflurane 1.2% (10 patients)or propofol 5 mg kg^–1 h^–1 with nitrous oxide 60%in oxygen (17 patients). Results. No CMAP were detected during isoflurane anaesthesia.During propofol anaesthesia 333 Hz, four-pulse magnetic stimulationevoked CMAP in the hypothenar muscle in 75%, and in the anteriortibial muscle in 65% of the patients. Less response was obtainedwith 250 and 200 Hz stimulation. Conclusions. In most patients, rTCMS can overcome suppressionof CMAP during propofol/nitrous oxide anaesthesia, but not duringisoflurane anaesthesia. A train of four magnetic stimuli ata frequency of 333 Hz is most effective in evoking potentialsfrom the upper and lower limb muscles. The authors concludethat rTCMS can be used for evaluation of the descending motorpathways during anaesthesia. Br J Anaesth 2003; 91: 487–92     

Unconscious auditory priming during surgery with propofol and nitrous oxide anaesthesia: a replication

Background. Priming during anaesthesia has been hard to replicateand the conditions under which it occurs remain poorly understood.We replicated and extended a recent study to determine whetherintraoperative priming during propofol and nitrous oxide anaesthesiais a reliable phenomenon, whether it occurs due to awarenessduring word presentation and whether it is suppressed by a doseof fentanyl at induction. Methods. Words were played through headphones during surgeryto 62 patients receiving propofol and nitrous oxide anaesthesia.Thirty-two patients received fentanyl 1.5 µg kg^–1at induction and 30 received no fentanyl. Neuromuscular blockingdrugs were not used. Depth of anaesthesia was measured usingthe bispectral index (BIS). Anaesthetic variables were recordedat 1 min intervals during word presentation. On recovery, implicitand explicit memory were assessed using an auditory word-stemcompletion test and a yes–no word-recognition test, respectively. Results. BIS, blood pressure, end-tidal carbon dioxide and heartrate during word presentation did not differ between the studygroups. The infusion rate of propofol and the patients' ventilatoryfrequency were significantly higher in the group not receivingfentanyl. No patient had unprompted explicit recall of surgery,although there was above-zero performance in six patients onthe yes–no recognition task (P<0.05). There was nophysiological evidence of awareness during anaesthesia (medianmean-BIS=38 in the no-fentanyl group and 42 in the fentanylgroup). There was evidence for priming (mean priming score=0.09,P<0.05 in the no-fentanyl study group; mean priming score=0.07,P<0.05 in the fentanyl group) even when patients with momentarylight anaesthesia (maximum recorded BIS     

A fine balance--one-lung ventilation in a patient with Eisenmenger syndrome

A 38-yr-old woman with an atrial septum defect and Eisenmengersyndrome was scheduled for a lung biopsy via thoracoscopy duringone-lung ventilation. Fluids were given to increase centralvenous pressure to 8 mm Hg, an epidural catheter was insertedat the sixth thoracic intervertebral space and ropivacaine 0.3%,6 ml were given. Careful balance of systemic and pulmonary vascularresistance is crucial in Eisenmenger syndrome, so norepinephrine(0.14 mg kg^–1 min^–1) was infused before generalanaesthesia was started with fentanyl 4 mg kg^–1, ketamine2 mg kg^–1, pancuronium 1 mg and succinylcholine 2 mg kg^–1.Anaesthesia was maintained with propofol 4–8 mg kg^–1h^–1. To control pulmonary artery pressure, ventilationwas performed with oxygen 100% and nitric oxide 20 ppm. Surgeryand anaesthesia course were uneventful and the patient was extubated.However, pleural haemorrhage required treatment with blood components,re-intubation on the second postoperative day and removal ofthe haematoma by mini-thoracotomy. A step-by-step approach usinga balanced combination of regional and general anaesthesia,controlled fluid administration, norepinephrine and inhalednitric oxide preserved a stable circulation even during one-lungventilation. The diagnostic value of lung biopsy must be weighedagainst the possibility of life-threatening haemorrhage. Br J Anaesth 2004; 92: 587–90     

Sevoflurane and propofol decrease intraocular pressure equally during non-ophthalmic surgery and recovery

Background. To provide good control of intraocular pressure(IOP) during anaesthesia and surgery, we conducted a study comparingthe effects on IOP during maintenance and recovery of sevofluranevs propofol anaesthesia in 33 patients (ASA I–II) undergoingelective non- ophthalmic surgery. Methods. Anaesthesia was induced with propofol 2 mg kg^–1,fentanyl 2 µg kg^–1 and vecuronium 0.1 mg kg^–1.Patients were allocated randomly to receive either propofol4–8 mg kg^–1 h^–1 (group P; n=16)or 1.5–2.5 vol% sevoflurane (group S; n=17) for maintenanceof anaesthesia. Fentanyl 2–4 µg kg^–1was added if necessary. The lungs were ventilated with 50% airin oxygen. Blood pressure, heart rate, oxygen saturation andend-tidal carbon dioxide were measured before and throughoutanaesthesia and in the recovery room. IOP was determined withapplanation tonometry (Perkins) by one ophthalmologist blindedto the anaesthetic technique. Results. There was a significant decrease in IOP after inductionand during maintenance of anaesthesia in both groups. No significantdifferences in IOP between the two groups was found. Conclusion. Sevoflurane maintains the IOP at an equally reducedlevel compared with propofol. Br J Anaesth 2002; 89: 764–6     

Sore throat and hoarseness after total intravenous anaesthesia

Background. Sore throat and hoarseness are common complications,but these have not been studied after total i.v. anaesthesia. Methods. We prospectively studied 418 surgical patients, aged15–92 yr, after total i.v. anaesthesia with propofol,fentanyl and ketamine to assess possible factors associatedwith sore throat and hoarseness. Result. We found sore throat in 50% and hoarseness in 55% ofpatients immediately after surgery. This decreased to 25% forsore throat and 24% for hoarseness on the day after surgery.Both sore throat and hoarseness were more common in femalesand when lidocaine spray had been used. Cricoid pressure duringlaryngoscopy was inversely associated with the risk of sorethroat. Conclusion. Knowledge of these factors may reduce postoperativethroat complications, and improve patient satisfaction. Br J Anaesth 2004; 92: 541–3     

Pharmacological effects of intravenous melatonin: comparative studies with thiopental and propofol

Background. Possible utility of high-dose i.v. melatonin asan anaesthetic adjuvant has not been studied. This study comparedits effects with thiopental and propofol. Methods. Sprague Dawley rats were assigned to receive bolusor cumulative i.v. doses of melatonin, thiopental or propofol.Righting reflex, hindpaw withdrawal to a noxious stimulus, responseto tail clamping and haemodynamic effects were assessed. Results. Melatonin caused a dose-dependent increase in paw withdrawalthreshold and the percent of rats displaying loss of the rightingreflex. Melatonin was comparable to thiopental and propofolin terms of its rapid onset of hypnosis. The mean ED₅₀ valuesfor loss of righting reflex were 5.4 (SEM 1.2), 12.5 (1.1) and178 (1.1) mg kg^–1 for propofol, thiopental and melatonin,respectively. The percent of rats displaying loss of responseto tail clamping was greater with propofol than with melatonin(P<0.05). Haemodynamic changes produced by melatonin or propofolwere similar in onset and magnitude. Conclusions. I.V. melatonin can exert hypnotic effects similarto those observed with thiopental and propofol. Melatonin exhibitedsignificant antinociceptive effects but was less effective inabolishing the response to tail clamping. Br J Anaesth 2003; 90: 504–7     

Ketamine, but not propofol, anaesthesia is regulated by metabotropic glutamate 5 receptors

Background. Group I metabotropic glutamate receptors (mGluRs)have been reported to regulate N-methyl-D-aspartate (NMDA) receptorfunction in various brain regions. The selective mGluR5 antagonist2-methyl-6-(phenylethynyl)-pyridine (MPEP) can potentiate NMDAantagonists such as PCP and MK-801-induced behavioural responses.In the present study, the role of group I mGluRs on ketamine-and propofol-induced general anaesthesia was examined. Methods. Mice were pretreated with various doses of the groupI mGluR agonist (S)-3,5-dihydroxyphenylglycine (DHPG), selectivemGluR5 agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG),mGluR1 antagonist 7-(hydroxyimino)cyclopropa[b]chromen-1a-carboxylateethyl ester (CPCCOEt) and mGluR5 antagonist MPEP followed byadministration of ketamine (120 mg kg^–1) or propofol (140mg kg^–1) to induce anaesthesia. The duration of loss ofrighting reflex was recorded. Results. DHPG and CHPG antagonized and MPEP potentiated ketamine-inducedanaesthesia in a dose-dependent manner. CPCCOEt was ineffective.However, propofol-induced anaesthesia was not affected aftermanipulating mGluR1 and mGluR5 receptors. Conclusions. mGluR5 receptors play an important role in modulationof anaesthesia induced by ketamine, but not propofol.     

Potentiation by ketamine of fentanyl antinociception. I. An experimental study in rats showing that ketamine administered by non-spinal routes targets spinal cord antinociceptive systems

Background. Ketamine has been found to exert antinociceptiveeffects in animals and to be analgesic at subanaesthetic dosesin humans. This study was designed to investigate the involvementof spinal cord mechanisms in the potentiation of opioid analgesiaby parenteral non-spinal administration of ketamine. Methods. Thresholds for nociception were measured in an acutepain model in rats that allowed identification of antinociceptiveeffects due to drug action in the spinal cord. Dose–responsecurves for the antinociceptive effects of ketamine alone andketamine in conjunction with the µ opioid fentanyl wereconstructed. Results. Intraperitoneal ketamine up to 3.75 mg kg^–1caused no sedative or antinociceptive effects and intrathecalketamine caused dose-dependent, spinally mediated antinociceptiveeffects. Injections of ketamine doses that caused no antinociceptiveeffects when given alone (intrathecal 25 µg and intraperitoneal3.75 mg/kg) significantly increased spinally mediated antinociceptionproduced by intrathecal fentanyl injections when assessed usingnoxious heat (tail-flick test) but not when assessed by noxiouselectrical current (electrical current threshold test). Conclusions. We conclude that ketamine can potentiate the effectsof fentanyl by an interaction at the level of the spinal cordeven when ketamine is given via a non-spinal route of administration. Br J Anaesth 2002; 88: 685–91     

Effects of magnesium sulphate and clonidine on propofol consumption, haemodynamics and postoperative recovery

Background. This placebo-controlled, double-blind study wasdesigned to assess the effects of magnesium sulphate and clonidineon peroperative haemodynamics, propofol consumption and postoperativerecovery. Methods. Sixty ASA I–II patients undergoing spinal surgerywere randomized into three groups. Group M received magnesiumsulphate 30 mg kg^–1 as a bolus before induction and 10mg kg^–1 h^–1 by infusion. Group CL received clonidine3 µg kg^–1 as a bolus before induction and 2 µgkg^–1 h^–1 by infusion during the operation period.The same volume of isotonic solution was administered to thecontrol group (group CT). Anaesthesia was induced with propofoland was maintained with propofol infusion [dose according tothe bispectral index (BIS)], fentanyl and cisatracurium. Analysisof variance and the Bonferroni test were used for statisticalanalysis. Results. Induction of anaesthesia with propofol was rapid inthe presence of magnesium sulphate and clonidine. The time forBIS to reach 60 was significantly shorter in group M and groupCL (P<0.0001) but postoperative recovery was slower withmagnesium sulphate compared with the clonidine and control groups(P<0.0001). There was no statistical difference in heartrate and arterial blood pressure between the groups. Propofolrequirements for induction and maintenance of anaesthesia weresignificantly lower with magnesium and clonidine (P<0.0001). Conclusion. Clonidine caused bradycardia and hypotension andmagnesium sulphate caused delayed recovery, but can be usedas adjuvant agents with careful management.     

Effect of clonidine pre-medication on propofol requirements during lower extremity vascular surgery: a randomized controlled trial

Background. Pre-medication with clonidine reduces the requirementfor volatile agents during general anaesthesia. This may alsobe true for anaesthesia with propofol, but the amount of dosereduction has not been measured. Because clonidine also affectscardiac output and thus regional blood flow it could alter thepharmacokinetics of propofol. This randomized, double-blindplacebo-controlled trial aimed to study the effect of clonidinepre-medication on dose requirement for propofol during lowerextremity vascular surgery using the bispectral index (BIS)as a measure of anaesthetic depth. Methods. After oral pre-medication with either clonidine 3 µgkg^–1 or placebo, 39 subjects had lower limb vascular surgeryusing propofol infusion for anaesthesia. Anaesthetic depth wasadjusted to a BIS of 45. Predicted plasma propofol concentrationswere noted every 30 min from a target-controlled propofol infusionpump and arterial samples were taken at the same time for propofolmeasurements. Results. Patients in both groups were anaesthetized to similardepths of anaesthesia as indicated by BIS readings (P=0.44).The groups had comparable mean (95% CI) arterial concentrationsof propofol, 4.8 (3.5–6.1) µg ml^–1 in thepatients given clonidine, and 4.6 (3.4–5.7) µg ml^–1in the patients given placebo (P=0.81). However, the averageplasma concentration predicted by the target-controlled infusionwas less in the clonidine group [3.2 (2.9–3.5)] than inthe group given placebo [3.6 (3.3–3.9)] µg ml^–1(P<0.05). Conclusions. Pre-medication with clonidine reduces the requirementfor propofol, which is a pharmacokinetic effect and not a pharmacodynamiccentral sedative effect.     

Comparison of the effects of sevoflurane and propofol on cooling and rewarming during deliberate mild hypothermia for neurosurgery

Background. Because the time available for cooling and rewarmingduring deliberate mild hypothermia is limited, studies of therate of the cooling and rewarming are useful. The decrease incore hypothermia caused by heat redistribution depends on theanaesthetic agent used. We therefore investigated possible differencesbetween sevoflurane and propofol on the decrease and recoveryof core temperature during deliberate mild hypothermia for neurosurgery. Methods. After institutional approval and informed consent,26 patients were assigned randomly to maintenance of anaesthesiawith propofol or sevoflurane. Patients in the propofol group(n=13) received propofol induction followed by a continuousinfusion of propofol 3–5 mg kg^–1 h^–1.Patients in the sevoflurane group (n=13) received propofol inductionfollowed by sevoflurane 1–2%. Nitrous oxide and fentanylwere also used for anaesthetic maintenance. After inductionof anaesthesia, patients were cooled and tympanic membrane temperaturewas maintained at 34.5°C. After surgery, patients were activelyrewarmed. Results. There was no difference in the rate of decrease andrecovery of core temperature between the groups. There was alsono difference in skin surface temperature gradient (forearmto fingertip), heart rate and mean arterial blood pressure betweenthe groups. Conclusions. Sevoflurane-based anaesthesia did not affect coolingand rewarming for deliberate mild hypothermia compared withpropofol-based anaesthesia. Br J Anaesth 2003; 90: 32–8     

Respiratory response to skin incision during anaesthesia with infusions of propofol and alfentanil

Background. The ventilatory response to skin incision duringanaesthesia with enflurane is an increase in tidal volume withouta change in frequency. As opioids affect respiratory frequencyand also affect the processing of pain, we investigated if thebreathing response to a painful stimulus could be differentduring anaesthesia using opioids. Methods. We studied 12 patients during anaesthesia with target-controlledinfusions of propofol (plasma target concentration 4–6 µg ml^–1)and alfentanil (plasma target concentration 40–60 ng ml^–1),having varicose vein surgery. Results. After the initial skin incision, tidal volume increasedpromptly by 17 (4, 81)% (median, quartile values) (P<0.01).Respiratory frequency changed variably with no significant changeoverall [median change 2 (–8, +50)%]. The duration ofinspiration was virtually unaltered, and the duration of expirationdecreased gradually by 5 (–7, 32)%. Patients who showedmore response also showed more change in tidal volume, so thatthere was a significant relationship between increased inspiratoryflow rate and reduced expiratory time (P<0.05). Conclusions. During opioid anaesthesia, the mechanism of ventilatoryincrease after stimulation involves changes in both drive andtiming of breathing. This pattern of response does not resemblethe changes seen during anaesthesia with potent volatile agents. Br J Anaesth 2002; 88: 649–52     

Evaluation of effects of magnesium sulphate in reducing intraoperative anaesthetic requirements

Background. The present randomized, placebo-controlled, double-blindstudy was designed to assess the effect of peroperatively administeredi.v. magnesium sulphate on anaesthetic and analgesic requirementsduring total i.v. anaesthesia. Methods. Eighty-one patients (36 women, 45 men) undergoing electivespinal surgery were included in one of two parallel groups.The magnesium group received magnesium sulphate 30 mg kg^–1as a bolus before induction of anaesthesia and 10 mg kg^–1h^–1 by continuous i.v. infusion during the operation period.The same volume of isotonic solution was administered to thecontrol group. Anaesthesia was maintained with propofol (administeredaccording to the bispectral index) and remifentanil (adjustedaccording to heart rate and arterial blood pressure) infusions. Results. A significant reduction in hourly propofol consumptionwas observed with magnesium administration. For example, themean infusion rate of propofol in the second hour of the operationwas 7.09 mg kg^–1 h^–1 in the controlgroup vs 4.35 mg kg^–1 h^–1 in themagnesium group (P<0.001). The magnesium group required significantlyless remifentanil (P<0.001) and vecuronium (P<0.001).No side-effects were observed with magnesium administration. Conclusion. The administration of magnesium led to a significantreduction in the requirements for anaesthetic drugs during totali.v. anaesthesia with propofol, remifentanil and vecuronium. Br J Anaesth 2002; 89: 594–8     

Recovery of elderly patients from two or more hours of desflurane or sevoflurane anaesthesia

Background. The solubility of desflurane compared with sevofluranesuggests more rapid recovery from desflurane anaesthesia. Thiscould be important after prolonged anaesthesia and fast recoverymay be advantageous in the elderly where slow recovery of mentalfunction is a concern. We compared emergence from desfluranevs sevoflurane in elderly patients undergoing two or more hoursof anaesthesia. Methods. Fifty ASA physical status I, II, or III patients, 65yr of age or older, undergoing anaesthesia expected to lasttwo or more hours were randomly assigned to receive desflurane/nitrousoxide or sevoflurane/nitrous oxide anaesthesia. Patients weregiven 1–2 µg kg^–1 fentanyl i.v. and anaesthesiawas induced with propofol 1.5–2.5 mg kg^–1 i.v. andmaintained with either desflurane 2–6% or sevoflurane0.6–1.75% with nitrous oxide 65% in oxygen. Inspired anaestheticconcentrations were adjusted to obtain adequate surgical anaesthesiaand to maintain mean arterial pressure within 20% of baselinevalues. Early and intermediate recovery times were recorded.Digit-Symbol Substitution Test (DSST) scores and Visual AnalogScale (VAS) scores for pain and nausea were recorded beforepre-medication and every 15 min in the Post Anaesthesia CareUnit (PACU) until patients were discharged. Results. Early recovery times are given as median, quartiles.The times to extubation (5 (4–9); 9 (5–13) min),eye opening (5 (3–5); 11 (8–16) min), squeezingfingers on command (7 (4–9); 12 (8–17) min); andorientation (7 (5–9); 16 (10–21) min) were significantlyless (P<0.05) for desflurane than for sevoflurane. Intermediaterecovery, as measured by the DSST and time to ready for dischargefrom the PACU (56 (35–81); 71 (61–81) min) was similarin the two groups. Conclusions. Early but not intermediate recovery times of elderlypatients undergoing a wide range of surgical procedures requiringtwo or more hours of anaesthesia is significantly (P     

Effect of a single dose of esmolol on the bispectral index scale (BIS) during propofol/fentanyl anaesthesia

Background. Esmolol, a short-acting ß₁-antagonist,can reduce anaesthetic requirements and decrease seizure activityduring electroconvulsive therapy even after a single dose of80 mg. We studied the effect of esmolol on the bispectralindex scale (BIS), which is a processed EEG recently introducedto monitor depth of anaesthesia. Methods. We gave esmolol 80 mg to 30 healthy male patientsafter induction of anaesthesia using propofol, with either fentanyl(group 1) or placebo (group 2). Patients were ventilated mechanicallythrough a laryngeal mask airway and anaesthesia was maintainedusing propofol to keep the BIS value between 55 and 60. Results. Esmolol did not affect the BIS index value in eithergroup. In group 1, the areas (mean (SD)) under the BIS vs timecurve 3 min before and 3 min after esmolol administrationwere 145 (9) and 146 (8) respectively (P=0.116). In group 2values were 147 (8) and 146 (7) respectively (P=0.344). In contrast,in group 1 the area under the systolic arterial pressure (SAP)curve was 299 (31) before and 270 (29) after esmolol (P<0.001),and 156 (17) and 141 (17) respectively for heart rate (P<0.001).In group 2 values were 326 (36) and 302 (41) for SAP (P<0.001)and 182 (25) and 155 (22) for heart rate (P<0.001). Conclusions. The results suggest that a single dose of esmololaffects the SAP and heart rate but does not affect BIS values. B J Anaesth 2002; 89: 509–11