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     

Effects of sevoflurane and propofol on ischaemia-reperfusion injury after thoracic-aortic occlusion in pigs

Background: Thoraco-abdominal-aneurysm surgery predicts high mortality.Propofol and sevoflurane are commonly used anaesthetics forthis procedure. Halogenated anaesthetics induce organ protectionsimilar to ischaemic preconditioning. We investigated whichanaesthetic regimen would lead to a better protection againstischaemia–reperfusion injury induced by temporary thoracic-aorticocclusion. Methods: Following initial fentanyl–midazolam anaesthesia for surgicalpreparation, 18 pigs were randomly assigned to two groups: groupone received propofol (n = 9) and group two sevoflurane (n =9) before, during, and after lower body ischaemia in an investigatorblinded fashion. Ten animals without aortic occlusion servedas time controls (propofol, n = 5; sevoflurane, n = 5). Forinduction of ischaemia, the thoracic aorta was occluded by aballoon-catheter for 90 min. After 120 min of reperfusion, thestudy anaesthetics were discontinued and fentanyl–midazolamre-established for an additional 180 min. Goal-directed therapywas performed during reperfusion. Fluid and catecholamine requirementswere assessed. Serum samples and intestinal tissue specimenswere obtained. Results: Severe declamping shock occurred in both study groups. Whilenorepinephrine requirements in the sevoflurane group were significantlyreduced during reperfusion (P < 0.05), allowing cessationof catecholamine support in 4/9 animals, all 9/9 animals werestill catecholamine dependent at the end of the experiment inthe propofol group. Serum activities of lactate dehydrogenase,aspartate transaminase, and alanine aminotransferase were lowerwith sevoflurane (P < 0.05). Small intestine tissue specimensdid not differ histologically. Conclusions: Use of sevoflurane compared with propofol attenuated the haemodynamicsequelae of reperfusion injury in our model. Release of serummarkers of cellular injury was also attenuated.     

Midazolam versus propofol for reducing contractility of fatigued canine diaphragm

The effects of midazolam and propofol on the contractility offatigued canine diaphragm were examined. Diaphragmatic fatiguewas induced by intermittent supramaximal bilateral electrophrenicstimulation at a frequency of 20 Hz applied for 30 min.After fatigue had been induced, group I (n=10) receivedno study drug, group II (n=10) was given a propofol infusion(0.1 mg kg^–1 loading dose plus 1.5 mg kg^–1 h^–1maintenance dose) and group III (n=10) was given a midazolaminfusion (0.1 mg kg^–1 loading dose plus 0.1 mg kg^–1 h^–1maintenance dose). Diaphragmatic contractility was assessedby measuring transdiaphragmatic pressure (P_di). After the fatigue-inducingperiod in each group, P_di at low-frequency (20 Hz) stimulationwas lower than the baseline values (P<0.05), whereas no changein P_di at high-frequency (100 Hz) stimulation was observed.In group II, P_di at 20 Hz stimulation was lower than fatiguedvalues (P<0.05); P_di at 100 Hz stimulation did not change.In group III, P_di at both stimulation frequencies was lowerthan fatigued values (P<0.05). Compared with group I, P_diat 20 Hz stimulation was lower than fatigued values (P<0.05)during administration of the study drug in groups II and III.The decrease in P_di was greater in group III than in group II(P<0.05). In conclusion, midazolam compared with propofolis associated with an inhibitory effect on contractility inthe fatigued canine diaphragm. Br J Anaesth 2001; 86: 879–81     

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.      

Loss of volition and pain response during induction of anaesthesia with propofol or sevoflurane

We compared the time to reach two anaesthetic end-points duringinduction of anaesthesia with a potent inhalation agent (sevoflurane)and an i.v. agent (propofol). We used a method to ensure steadybreathing during inhalation induction, and measured loss oftone in the outstretched arm and loss of response to a painfulstimulus. Thirty-eight female patients (age 39 (9) yr, weight65 (11) kg, and height 165 (8) cm) (mean (SD)) were randomlyallocated to receive either propofol or sevoflurane. The predictedinduction dose of propofol, estimated from age and weight foreach patient, was given at a rate of 1% of the induction doseper second, to a possible maximum of 2.5 times the predictedinduction dose. Sevoflurane was given with an inhaled concentrationof 8%, which was anticipated to cause loss of arm tone within90–120 s. After loss of consciousness, we applied a painfulelectrical stimulus to a finger at 15-s intervals and measuredthe time to loss of motor response. The median times and interquartilevalues for loss of arm tone were 105 (88–121) s for sevofluraneand 65 (58–80) s for propofol. This was equivalent to0.65 of the ED₅₀ of propofol. The time to loss of response topain was 226 (169–300) s for sevoflurane. The variancesof these three measurements were not significantly different,indicating that these dose–response relationships weresimilar. In contrast, only 11 of the patients given propofollost the response to pain after 2.5xED₅₀ had been given. Theseresults support previous evidence of substantial differencesbetween anaesthetic end-points, and show that this evidencecan be obtained using a simple and rapid method. Br J Anaesth 2001; 87: 283–6     

Anoxic depolarization of rat hippocampal slices is prevented by thiopental but not by propofol or isoflurane

Background. There is strong evidence to suggest that anoxicdepolarization (AD) is an important factor in hypoxia/ischaemia-inducedneural damage. Treatments that prevent the occurrence of ADmay be useful in providing neuronal protection against hypoxia.The current study was designed to determine whether generalanaesthetics which have been suggested to ‘induce prophylaxis’against hypoxia can attenuate the incidence of AD. Methods. The effects of anoxia (3 min) on evoked extracellularlyrecorded field potentials of CA1 neurons in rat hippocampalslices were assessed in the absence and presence of the i.v.general anaesthetics thiopental and propofol and the volatileanaesthetic isoflurane. Results. In the absence of anaesthetics, AD occurred in 81%of the preparations tested. Thiopental (2x10^–4 M) significantlyreduced the incidence of AD (16%, P=0.0006). In comparison,propofol (2x10^–4 M) and isoflurane (1.5 vol%) were ineffective(69% and 60%, respectively). Furthermore, in the presence ofthiopental, the population spike amplitude recovered with andwithout AD (90% and 94% of pre-anoxic value, respectively) following3 min anoxia. Conclusion. The prophylactic effect of thiopental against hypoxiamight be induced, in part, by preventing the generation of AD.     

Effects of propofol vs sevoflurane on arterial oxygenation during one-lung ventilation

Background: The inhibitory effect of anaesthetic agents on hypoxic pulmonaryvasoconstriction may depend upon their dose, especially whenusing a volatile agent. The aim of this randomized open studywas to compare the effects of sevoflurane and propofol, as primaryanaesthetic agents, on oxygenation during one-lung ventilation(OLV), with their administration being adjusted to maintainbispectral index (BIS) values between 40 and 60. Methods: Eighty patients scheduled for a lobectomy, receiving an epiduralmixture of ropivacaine and sufentanil, were randomly assignedto Group S (maintenance with sevoflurane) or Group P (maintenancewith propofol). After placement of a double-lumen tube, thelungs were ventilated at an inspiratory fraction of oxygen of1.0, a tidal volume of 6 ml kg^–1, and 12 bpm. Arterialblood gas samples were taken as follows: during two-lung ventilationbefore OLV, and during the first 40 min of OLV. Results: Fifteen patients were excluded (incorrect placement of the tubeor BIS outside the desired range). The two groups were comparablein terms of demographic variables, haemodynamic, and BIS levelsduring the operation. Four patients in each group had a Sp_O2<90%.Mean of the lowest Pa_O2 was 16.3 (7.5) kPa in Group S and 17.7(9.3) kPa in Group P (ns). Conclusions: Sevoflurane and propofol had similar effect on Pa_O2 during OLVwhen their administration is titrated to maintain BIS between40 and 60.     

Comparison of propofol/remifentanil and sevoflurane/remifentanil for maintenance of anaesthesia for elective intracranial surgery

Background. Propofol and sevoflurane are suitable agents formaintenance of anaesthesia during neurosurgical procedures.We have prospectively compared these agents in combination withthe short-acting opioid, remifentanil. Methods. Fifty unpremedicated patients undergoing elective craniotomyreceived remifentanil 1 µg kg^–1 followed by an infusioncommencing at 0.5 µg kg^–1 min^–1 reducing to0.25 µg kg^–1 min^–1 after craniotomy. Anaesthesiawas induced with propofol, and maintained with either a target-controlledinfusion of propofol, minimum target 2 µg ml^–1 orsevoflurane, initial concentration 2%_ET. Episodes of mean arterialpressure (MAP) more than 100 mm Hg or less than 60 mm Hg formore than 1 min were defined as hypertensive or hypotensiveevents, respectively. A surgical assessment of operating conditionsand times to spontaneous respiration, extubation, obey commandsand eye opening were recorded. Drug acquisition costs were calculated. Results. Twenty-four and twenty-six patients were assigned topropofol (Group P) and sevoflurane anaesthesia (Group S), respectively.The number of hypertensive events was comparable, whilst morehypotensive events were observed in Group S than in Group P(P=0.053, chi-squared test). As rescue therapy, more labetolol[45 (33) vs 76 (58) mg, P=0.073] and ephedrine [4.80 (2.21)vs 9.78 (5.59) mg, P=0.020] were used in Group S. Between groupdifferences in recovery times were small and clinically unimportant.The combined hourly acquisition costs of hypnotic, analgesic,and vasoactive drugs appeared to be lower in patients maintainedwith sevoflurane than with propofol. Conclusion. Propofol/remifentanil and sevoflurane/remifentanilboth provided satisfactory anaesthesia for intracranial surgery.     

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     

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.     

Effects of propofol and sevoflurane on the excitability of rat spinal motoneurones and nociceptive reflexes in vitro

Background. Spinal actions of halogenated ethers are widelyrecognized, whereas spinal actions of intravenous anaestheticslike propofol are less clear. The aim of this study was to comparethe spinal effects of propofol and sevoflurane. Methods. We used an isolated spinal cord in vitro preparationfrom rat pups and superfused the anaesthetics at known concentrations.Responses of motoneurones to single and repetitive C-fibre intensitystimulation (trains of 20 stimuli at 1 Hz) of a lumbar dorsalroot were recorded from the corresponding ventral root via asuction electrode. Results. Stimulation trains produced a wind-up of action potentialsin motoneurones. Both propofol and sevoflurane produced a significantconcentration-dependent depression of the evoked wind-up, althoughat clinically relevant concentrations sevoflurane exhibiteda larger intrinsic efficacy. Applied at anaesthetic concentrations,sevoflurane 250 µM abolished action potentials whereaspropofol 1 µM only produced a reduction close to 50%.At these concentrations, sevoflurane produced a large depressanteffect on the monosynaptic reflex whereas propofol was ineffective. Conclusions. Sevoflurane produces large inhibitory effects onnociceptive and non-nociceptive reflexes which are likely tocontribute to immobility during surgery. Compared with sevoflurane,propofol appears to have much weaker effects on spinal reflexessuch as those recorded in an isolated preparation.     

Desflurane compared with propofol for postoperative sedation in the intensive care unit

Background. We hypothesized that emergence from sedation inpostoperative patients in the intensive care unit would be fasterand more predictable after sedation with desflurane than withpropofol. Methods. Sixty patients after major operations were allocatedrandomly to receive either desflurane or propofol. The targetlevel of sedation was defined by a bispectral index^TM (BIS^TM)of 60. All patients were receiving mechanical ventilation ofthe lungs for 10.6 (SD 5.5) h depending on their clinical state.The study drugs were stopped abruptly in a calm atmosphere withthe fresh gas flow set to 6 litres min^–1, and the timeuntil the BIS increased above 75 was measured (t_BIS75, the mainobjective measure). After extubation of the trachea, when thepatients could state their birth date, they were asked to memorizefive words. Results. Emergence times were shorter (P<0.001) after desfluranethan after propofol (25th, 50th and 75th percentiles): t_BIS75,3.0, 4.5 and 5.8 vs 5.2, 7.7 and 10.3 min; time to first response,3.7, 5.0 and 5.7 vs 6.9, 8.6 and 10.7 min; time to eyes open,4.7, 5.7 and 8.0 vs 7.3, 10.5 and 20.8 min; time to squeezehand, 5.1, 6.5 and 10.2 vs 9.2, 11.1 and 21.1 min; time to trachealextubation, 5.8, 7.7 and 10.0 vs 9.7, 13.5 and 18.9 min; timeto saying their birth date, 7.7, 10.5 and 15.5 vs 13.0, 19.4and 31.8 min. Patients who received desflurane recalled significantlymore of the five words. We did not observe major side-effectsand there were no haemodynamic or laboratory changes exceptfor a more marked increase in systolic blood pressure afterstopping desflurane. Using a low fresh gas flow (air/oxygen1 litre min^–1), pure drug costs were lower for desfluranethan for propofol (95 vs 171 Euros day^–1). Conclusions. We found shorter and more predictable emergencetimes and quicker mental recovery after short-term postoperativesedation with desflurane compared with propofol. Desfluraneallows precise timing of extubation, shortening the time duringwhich the patient needs very close attention. Br J Anaesth 2003; 90: 273–80     

Effects of sevoflurane and propofol on left ventricular diastolic function in patients with pre-existing diastolic dysfunction

Background. The effects of anaesthetics on left ventricular(LV) diastolic function in patients with pre-existing diastolicdysfunction are not well known. We hypothesized that propofolbut not sevoflurane will worsen the pre-existing LV diastolicdysfunction. Methods. Of 24 randomized patients, 23 fulfilled the predefinedechocardiographic criterion for diastolic dysfunction. Theyreceived general anaesthesia with sevoflurane 1 MAC (n=12) orpropofol 4 µg ml^–1 (n=11). Echocardiographic examinationswere performed at baseline and in anaesthetized patients underspontaneous breathing and under positive pressure ventilation.Analysis focused on peak early diastolic velocity of the mitralannulus (E_a). Results. During spontaneous breathing, E_a was higher in thesevoflurane than in the propofol group [mean (95% CI) 7.0 (5.9–8.1)vs 5.5 (4.7–6.3) cm s^–1; P<0.05], reflectingan increase of E_a from baseline only in the sevoflurane group(P<0.01). Haemodynamic findings were similar in both groups,but the end-tidal carbon dioxide content was more elevated inthe propofol group (P<0.01). During positive pressure ventilation,E_a was similarly low in the sevoflurane and propofol groups[5.3 (4.2–6.3) and 4.4 (3.6–5.2) cm s^–1, respectively]. Conclusions. During spontaneous breathing, early diastolic functionimproved in the sevoflurane but not in the propofol group. However,during positive pressure ventilation and balanced anaesthesia,there was no evidence of different effects caused by the twoanaesthetics.     

Orally administered clonidine significantly reduces pain during injection of propofol

We examined the analgesic effects of orally administered clonidineon pain induced by injection of propofol (Diprivan; 2,6-diisopropylphenol). Female patients (n=81) were randomly allocated to oneof two groups: oral clonidine (5.5 µg kg^–1)followed by i.v. propofol and a control group given placebofollowed by i.v. propofol. The median pain score in the groupreceiving clonidine, using a four-point scale (0=no pain, 1=minimalpain, 2=moderate pain, 3=severe pain) was 1 (0–2), significantlylower than in the control group [2 (1–3), median (25–75percentiles), P<0.001]. Br J Anaesth 2001; 86: 874–6     

Sevoflurane anaesthesia in children after induction of anaesthesia with midazolam and thiopental does not cause epileptiform EEG

Background. Sevoflurane is a methyl ether anaesthetic commonlyused for induction and maintenance of general anaesthesia inchildren. Sevoflurane is a non-irritant and acts quickly soinduction is usually calm. However, inhalation induction withhigh concentrations of sevoflurane can cause convulsion-likemovements and seizure-like changes in the electroencephalogram(EEG). Little is known about the EEG during maintenance of anaesthesiawith sevoflurane, so we planned a prospective trial of sevofluranemaintenance after i.v. induction with benzodiazepine and barbiturate,which is another common induction technique in children. Methods. EEG recordings were made before premedication withmidazolam (0.1 mg kg^–1 i.v.), during induction ofanaesthesia with thiopental (5 mg kg^–1), and duringmaintenance with sevoflurane (2% end-tidal concentration inair/oxygen without nitrous oxide) in 30 generally healthy, 3-to 8-year-old children having adenoids removed. Noise-free EEGdata of good quality were successfully recorded from all 30children. Results. Two independent neurophysiologists did not detect epileptiformdischarges in any of the recordings. Conclusion. Premedication with midazolam, i.v. induction withthiopental and maintenance of anaesthesia with 2% sevofluranein air does not cause epileptiform EEG patterns in children. Br J Anaesth 2002; 89: 853–6     

Predicted values of propofol EC50 and sevoflurane concentration for insertion of laryngeal mask Classic and ProSeal

Background. A new laryngeal mask airway, the ProSeal^TM (PLMA),is said to be more difficult to insert than the laryngeal maskairway Classic^TM (CLMA) using propofol anaesthesia. Therefore,we expected a greater dose of propofol and sevoflurane to berequired to insert the PLMA compared with the CLMA. We determinedthe effective concentration 50% (EC₅₀) of propofol and end-tidalsevoflurane to allow insertion of the PLMA and the CLMA. Methods. Seventy-six elective female patients (aged 20–60yr and ASA I–II) were randomly assigned to one of fourgroups. Either a PLMA or a CLMA was inserted using either propofoltarget controlled infusion or sevoflurane. Both propofol andsevoflurane targets were determined with a modified Dixon’sup-and-down method. After equilibration between the predeterminedblood and effect site concentrations, which had been held steadyfor more than 10 min, LMA insertion was attempted without neuromuscularblock. Results. The predicted EC_50CLMA and EC_50PLMA for propofol were3.14 (0.33) and 4.32 (0.67) µg ml^–1. E'_CLMAand E'_PLMA of sevoflurane (mean (SD)) were 2.36 (0.22) and 2.82(0.45)% (P<0.01 and 0.05, respectively). Conclusions. The estimated concentration of propofol and thesevoflurane concentration needed to allow insertion of the ProSeal^TMare respectively 38 and 20% greater than those needed for insertionof the Classic LMA. Br J Anaesth 2004; 92: 242–5     

Effects of sevoflurane and propofol on pulmonary shunt fraction during one-lung ventilation for thoracic surgery

Forty patients requiring one-lung ventilation (OLV) for thoracicsurgery were randomly assigned to receive propofol (4-6 mg kg^–1h^–1) or sevoflurane (1 MAC) for maintenance of anaesthesia.Three sets of measurements were taken: (i) after 30 min of two-lungventilation (TLV), (ii) after 30 min of one-lung ventilation(OLV-1) in the supine position and (iii) during OLV in the lateralposition (OLV-2) with the chest open and before surgical manipulationof the lung. There were no differences between groups in patientcharacteristics or preoperative condition. Increases in shuntfraction during OLV-1 were 17.4% and 17.2% (P=0.94), those duringOLV-2 were 18.3% and 16.5% (P=0.59) for the propofol and sevofluranegroup, respectively. Cardiac index and other haemodynamic andrespiratory variables were similar for the two groups. We concludethat inhibition of hypoxic pulmonary vasoconstriction by sevofluranemay only account for small increases in shunt fraction and thatmuch of the overall shunt fraction during OLV has other causes. Br J Anaesth 2001; 86: 38–43     

Effect of propofol on twitch diaphragmatic pressure evoked by cervical magnetic stimulation in patients

Background: Several studies have demonstrated the inhibitory effect of propofolon diaphragmatic contractility in laboratory animals, but therehave been few studies in humans. We have investigated the effectof a single bolus injection of propofol on twitch diaphragmaticpressure (TwPdi) evoked by cervical supramaximal magnetic stimulation,and its impact on diaphragmatic contractility. Methods: In 16 patients scheduled for elective operation, TwPdi was evokedbilaterally at the cervical phrenic nerves with supramaximalmagnetic stimulations using a 140 mm diameter magnetic coil.Changes of TwPdi were monitored dynamically before and duringgeneral anaesthesia induced by single bolus of propofol 2 mgkg ^–1. During the study, all patients breathed 100% oxygenby a face mask, maintaining Sp_O2 99% and PE'_CO2 4.6–5.2kPa. Results: TwPdi declined after administration of propofol with gradualrecovery. Compared with baseline [20.6 (6.0) cm H₂O], TwPdidecreased by 23.3% (P<0.001) to [15.8 (6.4) cm H₂O]. Whenthe patients regained awareness, TwPdi returned to [19.1 (6.1)cm H₂O], close to baseline (P=0.063). The time from startingthe propofol infusion to the lowest TwPdi was [240 (86) s].Total time course of stimulation lasted [363 (89) s]. Conclusions: A single bolus propofol depressed TwPdi evoked by cervical magneticstimulation, demonstrating inhibitory effects of propofol ondiaphragmatic contractility in patients during general anaesthesia.     

Cerebrospinal fluid and blood propofol concentration during total intravenous anaesthesia for neurosurgery

Background. The aim of this paper is to compare the propofolconcentration in blood and cerebrospinal fluid (CSF) in patientsscheduled for different neurosurgical procedures and anaesthetizedusing propofol as part of a total intravenous anaesthesia technique. Methods. Thirty-nine patients (ASA I–III) scheduled forelective intracranial procedures, were studied. Propofol wasinfused initially at 12 mg kg^–1 h^–1 and thenreduced in steps to 9 and 6 mg kg^–1 h^–1. Duringanaesthesia, bolus doses of fentanyl and cis-atracurium wereadministered as necessary. After tracheal intubation the lungswere ventilated to achieve normocapnia with an oxygen-air mixture(FI_O2=0.33). Arterial blood and CSF samples for propofol examinationwere obtained simultaneously directly after intracranial drainageinsertion and measured using high-performance liquid chromatography.The patients were divided into two groups depending on the typeof neurosurgery. The Aneurysm group consisted of 13 patientswho were surgically treated for ruptured intracranial aneurysm.The Tumour group was composed of 26 patients who were undergoingelective posterior fossa extra-axial tumour removal. Results. Blood propofol concentrations in both groups did notdiffer significantly (P>0.05). The propofol concentrationin CSF was 86.62 (SD 37.99) ng ml^–1 in the Aneurysm groupand 50.81 (26.10) ng ml^–1 in the Tumour group (P<0.005). Conclusions. Intracranial pathology may influence CSF propofolconcentration. However, the observed discrepancies may alsoresult from quantitative differences in CSF composition andfrom restricted diffusion of the drug in the CSF. Br J Anaesth 2003; 90: 84–6     

Effects of ketamine and propofol on inflammatory responses of primary glial cell cultures stimulated with lipopolysaccharide

Background. Ketamine has been reported to exert anti-inflammatoryeffects on macrophages stimulated with lipopolysaccharide (LPS)in vitro and in vivo. Several studies have reported conflictingresults regarding the effects of propofol on cytokine productionfrom immune cells. However, there have been no reports of theeffects of these agents on inflammatory responses in glial cells.We investigated the effects of ketamine and propofol on LPS-inducedproduction of nitric oxide, tumour necrosis factor-