Corresponding minimum alveolar concentrations of isoflurane and isoflurane/nitrous oxide have divergent effects on thalamic nociceptive signalling

BACKGROUND: Suppression of nociceptive signalling in the thalamus is consideredto contribute significantly to the anaesthetic state. Assumingadditivity of anaesthetic mixtures, our study assessed the effectsof corresponding minimum alveolar concentrations (MACs) of isofluraneand isoflurane/nitrous oxide on thalamic nociceptive signalling. METHODS: Nociceptive response activity (elicited by controlled radiantheat stimuli applied to cutaneous receptive fields) of singlethalamic neurons was compared in rats anaesthetized at 1.1 and1.4 MAC isoflurane with that at 1.1 and 1.4 MAC isoflurane/nitrousoxide. RESULTS: Under baseline anaesthesia (0.9 MAC isoflurane), noxious stimulationelicited excitatory responses in all neurons (n = 19). Theseresponses were uniformly suppressed at 1.1 and 1.4 MAC isoflurane.In contrast, at 1.1 and 1.4 MAC isoflurane/nitrous oxide, excitatoryresponses no different to baseline were still present in 64and 37% of the neurons, respectively. CONCLUSIONS: These data demonstrate a pronounced nitrous oxide-induced responsevariability. It appears that, with respect to thalamic transferof nociceptive information, the interaction of isoflurane andnitrous oxide may not be compatible with the concept of additivityand that the antinociceptive potency of nitrous oxide is considerablyless than previously reported.     

Influence of sepsis on sevoflurane minimum alveolar concentration in a porcine model

Sevoflurane is widely used in anaesthetic protocols for patientsundergoing surgical procedures. However, there are no reportson the influence of sepsis on minimum alveolar concentrationof sevoflurane (MAC_SEV) in animals or in humans. The aim ofthis study was to test the hypothesis that sepsis could alterthe MAC_SEV in a normotensive septic pig model. Twenty young,healthy pigs were used. After they had received 10 mg kg^–1of ketamine i.m. for premedication, anaesthesia was establishedwith propofol 3 mg kg^–1 and the trachea wasintubated. Sevoflurane was used as the sole anaesthetic agent.Baseline haemodynamic recording included electrocardiography,carotid artery blood pressure and a pulmonary thermodilutioncatheter. Baseline MAC_SEV in each pig was evaluated by pinchingwith a haemostat applied for 1 min to a rear dewclaw. MAC_SEVwas determined using incremental changes in sevoflurane concentrationuntil purposeful movement appeared. Pigs were assigned randomlyto two groups: the saline group (n=10) received a 1-h i.v. infusionof sterile saline solution while the sepsis group (n=10) receiveda 1-h i.v. infusion of live Pseudomonas aeruginosa. Epinephrineand hydroxyethylstarch were used to maintain normotensive andnormovolemic haemodynamic status. In both groups, MAC_SEV wasevaluated 5 h after infusion. Significant increases inmean artery pulmonary pressure, filling, epinephrine and vascularpulmonary resistances occurred in the sepsis group. MAC_SEV forthe saline group was 2.4% [95% confidence interval (CI) 2.1–2.55%]and the MAC_SEV for the sepsis group was 1.35% (95% CI 1.2–1.45%,P<0.05). These data indicate that MAC_SEV is significantlydecreased in this normotensive septic pig model. Br J Anaesth 2001; 86: 832–6     

Minimum alveolar concentration of halogenated volatile anaesthetics in left ventricular hypertrophy and congestive heart failure in rats

BACKGROUND: Although many physiological and pathological conditions affect minimal alveolar concentration (MAC), there are no reliable data on the MAC for halogenated anaesthetics during left ventricular hypertrophy (LVH) and congestive heart failure (CHF). The aim of this experimental study was to determine the MAC values of halothane, isoflurane, and sevoflurane in rats, at early and later stages of cardiomyopathic hypertrophy. METHODS: LVH was induced by ascending aortic stenosis in 3-4-week-old rats. LVH and CHF in each animal were assessed weekly by echocardiography. MAC of halothane, isoflurane, and sevoflurane was determined using the tail-clamp technique in spontaneously breathing rats from each group. Response vs no-response data were analysed using logistic regression analysis. Data are medians (95% confidence interval). RESULTS: The MAC of halothane [1.30% (1.26-1.34)], isoflurane [1.52% (1.48-1.57)], and sevoflurane [2.93% (2.78-3.07)] in rats with LVH was not different from sham-operated rats [respectively, 1.23% (1.20-1.26), 1.52% (1.47-1.56), and 2.90% (2.79-3.00)]. Conversely, the MAC of halothane [1.44 (1.39-1.50)] and isoflurane [1.74 (1.69-1.78)], but not sevoflurane [2.99 (2.93-3.06)], was significantly increased in rats with CHF. CONCLUSIONS: MAC values for halothane, isoflurane, and sevoflurane were unchanged in rats with pressure-induced overload LVH. Conversely, the MAC for halothane and isoflurane, but not sevoflurane, was significantly increased in rats with CHF.     

Age-related iso-MAC charts for isoflurane,sevoflurane and desflurane in man

Background. The motivation for this study was the current difficultyin estimating the total age-related MAC for a patient in a clinicalsetting. Methods. Age-related iso-MAC charts for isoflurane, sevofluraneand desflurane were developed for the clinically useful MACrange (0.6–1.6), age range 5–95 yr, and put in aconvenient form for use by practising anaesthetists. The chartsare based on Mapleson’s meta-analysis (1996) of the availableMAC data and can be used to allow for the contribution of nitrousoxide to the total MAC. Results. The charts indicate the influence of age on anaestheticrequirements, showing, for example, that a total MAC of 1.2using isoflurane and nitrous oxide 67% in oxygen requires anend-expired isoflurane concentration of only 0.25% in a patientof 95 yr vs 1% in a 5-yr-old patient. Colleagues found the chartsto be helpful and simple to use clinically. Conclusions. The iso-MAC charts show clearly how patient agecan be used to guide the choice of end-expired agent concentration.They also allow a consistent total MAC to be maintained whenchanging the inspired nitrous oxide concentration, thereby reducingthe chance of inadvertent awareness, particularly at the extremesof age. Br J Anaesth 2003; 91: 170–4     

Inhibition of glutamate transporters increases the minimum alveolar concentration for isoflurane in rats

Background. Glutamate transporters [also named excitatory aminoacid transporters (EAATs)] bind and take up extracellular glutamate,a major excitatory neurotransmitter, and can regulate glutamatergicneurotransmission in synapses. As anaesthesia is proposed tobe induced by enhancing inhibitory neurotransmission, inhibitingexcitatory neurotransmission, or both we hypothesize that inhibitionof EAAT activity can increase the anaesthetic requirement. Methods. The minimum alveolar concentration (MAC, the anaestheticconcentration required to suppress movement in response to noxiousstimulation in 50% of subjects) for isoflurane was determinedin adult male Sprague–Dawley rats after intrathecal administrationof EAAT inhibitors. Results. Application of DL-threo-ß-benzyloxyaspartate,a selective EAAT inhibitor, dose- and time-dependently increasedthe MAC for isoflurane. The MAC was 109 (1)% and 116 (4)% ofthe baseline, respectively, for 0.2 and 0.4 µmol of DL-threo-ß-benzyloxyaspartate15 min after the injection of the drug (n=5, P<0.05 comparedwith the baseline MAC). Intrathecal injection of dihydrokainate,a selective inhibitor of EAAT type 2, also increased the MACfor isoflurane. Conclusions. These results suggest that EAAT in the spinal cordcan regulate the requirement of isoflurane to induce immobility.EAAT2 may be involved in this effect.     

Optimal concentration of epidural fentanyl in bupivacaine 0.1% after thoracotomy

Background. The aim of this prospective, double-blind, randomizedcontrolled trial was to investigate the analgesic and adverseeffects of three commonly used concentrations of thoracic epiduralfentanyl with bupivacaine in patients undergoing thoracotomyfor lung resection. Methods. We studied 99 patients who were randomized to receivefentanyl 2 µg ml^–1 (group 2), fentanyl 5 µgml^–1 (group 5) and fentanyl 10 µg ml^–1 (group10) in bupivacaine 0.1% via a thoracic epidural. Postoperatively,pain on coughing was assessed using a visual analogue scale(VAS) and an observer verbal rating score (OVRS) at 2, 8, 16and 24 h. At the same times, sedation, pruritus and nausea wereassessed. Results. Of 29, 28 and 32 patients who completed the study ingroups 2, 5 and 10 respectively, there was no significant differencein baseline characteristics between the three groups. The numberof patients with episodes of unsatisfactory pain, i.e. VAS scores>30 mm and OVRS >1, at each of the four assessments postoperativelywas significantly (P<0.01) higher in group 2 than in groups5 and 10. In group 10, 16 patients had sedation scores >1compared with 10 each in groups 2 and 5. In addition, 19 patientsin group 10 experienced pruritus compared with 12 each, in groups2 and 5. These differences were not significant. Nausea wasnot significantly different between the three groups. Conclusion. We conclude that thoracic epidural fentanyl 5 µgml^–1 with bupivacaine 0.1% provides the optimum balancebetween pain relief and side effects following thoracotomy. Br J Anaesth 2004: 92: 670–4     

Optimization of desflurane administration in morbidly obese patients: a comparison with sevoflurane using an 'inhalation bolus' technique

Background. The concept of an ‘inhalation bolus’can be used to optimize inhaled drug administration. We investigatedthe depth of anaesthesia, haemodynamic stability, and recoverytime in morbidly obese patients resulting from bispectral index^TM(BIS^TM)-guided sevoflurane or desflurane administration andBIS-triggered inhalation boluses of sevoflurane or desfluranecombined with titration of remifentanil. Methods. Fifty morbidly obese patients undergoing laparoscopicgastroplasty received either BIS-guided sevoflurane or desfluraneanaesthesia in combination with a remifentanil target-controlledinfusion. Intraoperative haemodynamic stability and BIS controlwere measured. Immediate recovery was recorded. Results. Intraoperatively, the BIS was between 40 and 60 fora greater percentage of time in the sevoflurane (78 (13)% ofcase time) than in the desflurane patients (64 (14)% of casetime), owing to too profound anaesthesia in the desflurane patientsat the start of the procedure. However, fewer episodes of hypotensionwere found in the desflurane group, without the occurrence ofmore hypertensive episodes. During immediate recovery, eye opening,extubation, airway maintenance, and orientation occurred soonerin the desflurane group. Conclusions. Immediate recovery was significantly faster inthe desflurane group. Overall hypnotic controllability measuredby BIS was less accurate with desflurane. Overall haemodynamiccontrollability was better when using desflurane. Fewer episodesof hypotension were found in the desflurane group. The use ofthe inhalation bolus was found to be appropriate in both groupswithout causing severe haemodynamic side effects. Minimal BISvalues were significantly lower after a desflurane bolus. Br J Anaesth 2003; 91: 638–50     

Blood/gas partition coefficients of halothane,isoflurane and sevoflurane in horse blood

Background. Blood/gas partition coefficients (_b/g) for volatileagents in horse blood are reported for halothane but not forisoflurane and sevoflurane. We measured the _b/g of halothane,isoflurane and sevoflurane in the blood of fasted horses. Thecorrelation with age, weight and some haematological and biochemicalvariables was studied. The temperature correction factor forisoflurane solubility was calculated. Methods. Twenty-four horses were randomly allocated to halothane(n=8), isoflurane (n=8) or sevoflurane (n=8). Blood sampleswere taken after 10 h’ fasting. Calculation of _b/g wasbased on the measurement of anaesthetic partial pressures inblood at 37 °C, which was achieved with tonometer equilibrationand headspace gas chromatography. Results. Mean _b/g was 1.66 (SD 0.06) for halothane, 0.92 (0.04)for isoflurane, and 0.47 (0.03) for sevoflurane. The _b/g valueswere all significantly lower than in humans (P<0.001). Nocorrelation was found between _b/g and weight, age, haematocrit,plasma triglycerides, cholesterol or total bilirubin. The changein isoflurane solubility per 1 °C temperature increase was–2.63 (0.13)%. Conclusion. The _b/g values of halothane, isoflurane and sevofluranein fasted horses are significantly lower than those reportedin humans. The _b/g for halothane in this study agrees with valuesreported in the literature but a positive correlation with plasmatriglycerides could not be confirmed. Knowledge of _b/g can refinemodels of anaesthetic uptake. Br J Anaesth 2003; 91: 276–8     

Model-based automatic feedback control versus human control of end-tidal isoflurane concentration using low-flow anaesthesia

We studied the clinical use of an automatic feedback controlsystem to adjust the end-tidal anaesthetic concentration witha low-flow method. The end-tidal controller uses two input signals(the end-tidal and inspiratory concentrations) to control theisoflurane concentration in the fresh gas flow, using a model-basedalgorithm. We studied 22 ASA I–III patients during electivesurgery lasting more than 2 h. The anaesthetist was askedto make four step changes of the target end-tidal concentration(+0.3, +0.6, –0.3, –0.6 vol%), either manually (GroupA) or by setting the target value for the feedback controller(Group B), and then the control was changed and the step changeswere repeated, in a crossover design. Eighty step changes witheach control method were compared in terms of response time,maximal overshoot and stability. The automatic control systemwas more accurate and stable than the human controller for stepincreases and step decreases, with less overshoot/undershootand greater stability [e.g. maximal overshoot 14.7 (SD 3.7)%and 18 (8.1)% respectively for +0.6 vol% step changes, and 19.8(3.7)% and 30.7 (13.2)% respectively for +0.3 vol% step changes].However, the automatic control system showed a faster responsetime than the manual method only with large increasing steps(e.g. 149 (32) s and 205 (57) s respectively for +0.6 vol%step changes) and was not different from manual control fordecreasing steps. Automatic control of the end-tidal isofluraneconcentration can be better than human control in a clinicalsetting, and this task could be done automatically. Br J Anaesth 2000; 85: 818–25     

Model-based administration of inhalation anaesthesia. 2. Exploring the system model

We explored our model by displaying its new capabilities, testingits sensitivity to variations in input data and illustratingits use. Its multiple-gas character allows simulation of themechanisms governing concentration and second gas effects. Simulatingthe volume of a standing bellows makes it possible to test algorithmsfor automated closed-circuit anaesthesia. Using desflurane,the model’s sensitivity to changes in blood/gas partitioncoefficient (range 0.42–0.576), cardiac output and minuteventilation was analysed. The model was very sensitive to changesin blood solubility; other results agreed with those reportedpreviously. An alveolar isoflurane tension of 1% atm was rapidlyattained and maintained, even using 0.5 litres min^–1 offresh gas, when isoflurane was ‘co-administered’through a vaporizer set to 3.5 vol% and a single aliquot (1.25ml liquid) injected into the expiratory limb. As a result ofits credibility and capabilities, the model is to be testedin the clinical setting. Br J Anaesth 2001; 86: 29–37     

Phase behaviour of premixed 0.25% isoflurane in 50% nitrous oxide and 50% oxygen

Background. Isoflurane (0.25%) in premixed nitrous oxide andoxygen 50/50, v/v, (IN₂O), has been suggested for pain reliefin labour. Methods. Possible phase separation of this mixture was studiedby analysis of samples from pre-filled cylinders as they werecooled. Results. Condensation of isoflurane was found at 3.1°Cin a cylinder, which held 8.7 MPa at 15°C. In a cylinderholding 13.8 MPa, which is the standard filling pressure stipulatedby the National Health Service, the condensation temperaturewas –2.3°C. At the highest cylinder filling pressureinvestigated (14.15 MPa) the separation temperature was evenless, –3.0°C. After exposure of cylinders to –40°Cand complete phase separation of the mixture, complete mixingwas achieved by 24 h storage in the horizontal position at roomtemperature and, either three complete inversions of the cylinderor mechanical rolling at 30 r.p.m. Conclusions. These findings should assist the use and storageof IN₂O. Br J Anaesth 2002; 89: 814–19     

The Bispectral Index in children: comparing isoflurane and halothane

Background. The Bispectral Index (BIS) has been calibrated forseveral general anaesthetic agents including isoflurane. Halothaneis still used in paediatric anaesthesia. Compared with othervolatile anaesthetics, halothane has a different receptor affinityand differing effects on the EEG. There are limited data evaluatingthe BIS with halothane. We set out to compare the BIS usinghalothane and isoflurane at a clinically relevant equipotentconcentration (1 MAC) and at a reproducible measure of anaestheticeffect (awakening). Methods. Forty children aged between 2 and 15 yr were enrolledin a masked randomized trial—20 in each group. Anaesthesiawas induced with sevoflurane or propofol. Either halothane orisoflurane were given to obtain an end-tidal concentration of1 MAC for 15 min. The BIS was then recorded. The BIS was alsorecorded at awakening. Values (mean (SD)) were compared witha t test. Results. At 1 MAC the BIS for halothane was significantly greaterthan isoflurane (56.5 (8.1) vs 35.9 (8.5), P<0.0001). Atawakening there was no significant difference (BIS halothane;81.1 (11.9), BIS isoflurane; 82.5 (16.4)). The difference inmeans at awakening was 1.4 (95% CI –8.2 to 11.1). Conclusions. At equipotent concentrations of halothane and isofluraneBIS valves were significantly greater with halothane. At awakeningthe BIS values were equivalent for each agent. This findingis consistent with the BIS being more affected by the agentused at higher concentrations of anaesthetic. The BIS must beinterpreted with caution when using halothane. Br J Anaesth 2004; 92: 14–17     

Small dose of clonidine mixed with low-dose ropivacaine and fentanyl for epidural analgesia after total knee arthroplasty

Background. We studied whether a small dose of clonidine addedto a ropivacaine–fentanyl mixture improves epidural analgesiawithout provoking side effects typically related to larger amountsof epidural clonidine. Methods. In this randomized, double-blinded study, patients(     

Epidural anaesthetic effect of the 8% emulsified isoflurane: a study in rabbits

BACKGROUND: Studies have shown that local use of volatile anaesthetics produce local anaesthetic effects such as local infiltration anaesthesia (in rats and humans) and spinal anaesthesia (in dogs). However, there is still no report on the epidural anaesthetic effect of volatile anaesthetics. The aim of the present study was to evaluate the epidural anaesthetic effect of the 8% emulsified isoflurane in rabbits. METHODS: Forty rabbits chronically instrumented with an epidural catheter were randomly divided into four groups of 10 rabbits each. According to group assignment, rabbits received epidural administration of 8% emulsified isoflurane (v/v) 1 ml in the E-isoflurane group, 1% lidocaine 1 ml in the Lidocaine group, 30% lipid emulsion 1 ml in the Itralipid group, or normal saline 1 ml in the NS group. The sensory and motor functions and the state of consciousness were assessed at baseline and at predetermined regular intervals. Then, the rabbits were continuously observed for 2 weeks to examine the possible long-term neurological complications. RESULTS: The sensory blockade onset time, motor blockade onset time, and motor blockade duration in the E-isoflurane group [1.4 (0.7), 1.6 (0.7), and 34 (10) min, respectively] were similar to those in the Lidocaine group [1.3 (0.5), 1.7 (0.8), and 38 (8), min, respectively]. The sensory blockade duration in the E-isoflurane group was longer than that in the Lidocaine group [68 (13) vs 49 (13) min, P<0.01]. No epidural anaesthetic effects occurred in the NS group and the Intralipid group. None of the rabbits showed an abnormal consciousness after the epidural drug administration. None of the rabbits showed any long-term neurological deficits during a 2 week observation. CONCLUSIONS: The present study demonstrates that epidural administration of the 8% emulsified isoflurane produces completely a reversible epidural anaesthetic effect that does not affect the level of consciousness in rabbits.     

Measuring the costs of inhaled anaesthetics

The cost of inhalation anaesthesia has received considerablestudy and is undoubtedly reduced by the use of low fresh gasflows. However, comparison between anaesthetics of the economiesachievable has only been made by computer modelling. We havecomputed anaesthetic usage for MAC-equivalent anaesthesia withisoflurane, desflurane, and sevoflurane in closed and open breathingsystems. We have compared these data with those derived duringclinical anaesthesia administered using a computer-controlledclosed system that measures anaesthetic usage and inspired concentrations.The inspired concentrations allow the usage that would haveoccurred in an open system to be calculated. Our computed predictionslie within the 95% confidence intervals of the measured data.Using prices current in our institution, sevoflurane and desfluranewould cost approximately twice as much as isoflurane in opensystems but only about 50% more than isoflurane in closed systems.Thus computer predictions have been validated by patient measurementsand the cost saving achieved by reducing the fresh gas flowis greater with less soluble anaesthetics. Br J Anaesth 2001; 87: 559–63     

Differential effects of halothane and isoflurane on lumbar dorsal horn neuronal windup and excitability

Background. Windup of spinal nociceptive neurones may underlietemporal summation of pain, influencing the minimum alveolarconcentration (MAC) of anaesthetics required to prevent movementto supramaximal stimuli. We hypothesized that halothane andisoflurane would differentially affect windup of dorsal hornneurones. Methods. We recorded 18 nociceptive dorsal horn neurones exhibitingwindup to 1 Hz electrical hindpaw stimuli in rats. Effects of0.8 and 1.2 MAC isoflurane and halothane were recorded in thesame neurones (counterbalanced, crossover design). Windup wascalculated as the total number of C-fibre (100–400 mslatency) plus afterdischarge (400–1000 ms latency) spikes/20stimuli (area under curve, AUC) or absolute windup (C-fibreplus afterdischarge–20xinitial response). Results. Increasing isoflurane from 0.8 to1.2 MAC did not affectAUC, but increased absolute windup from 429 (62) to 618 (84)impulses/20 stimuli (P<0.05) and depressed the initial C-fibreresponse from 14 (3) to 8 (2) impulses (P<0.05). Increasinghalothane from 0.8 to1.2 MAC depressed AUC from 690 (79) to537 (65) impulses/20 stimuli (P<0.05) and the initial responsefrom 18 (2) to 13 (2) impulses (P<0.05), but absolute windupwas not affected. Absolute windup was 117% greater during 1.2MAC isoflurane compared with 1.2 MAC halothane. Conclusions. Windup was significantly greater under isofluranethan halothane anaesthesia at 1.2 MAC, whereas the initial C-fibreresponse was suppressed more by isoflurane. These findings suggestthat these two anaesthetics have mechanistically distinct effectson neuronal windup and excitability.     

A prospective, double-blind, randomized trial of caudal block using ropivacaine 0.2% with or without fentanyl 1 microg kg-1 in children

Background. It has been reported that ropivacaine produces vasoconstrictionin contrast to vasodilation produced by bupivacaine. It is possiblethat additives to ropivacaine can provide further analgesicadvantages compared with bupivacaine. We thus evaluated whetherthe addition of fentanyl to ropivacaine prolonged the durationof analgesia after a single shot caudal block. Methods. A total of 36 children undergoing surgical proceduresbelow the umbilicus were randomly allocated to one of two groups:Group F received ropivacaine 0.2%, 1 ml kg^–1 with fentanyl1 µg kg^–1 and Group S received ropivacaine 0.2%,1 ml kg^–1 with saline. The analgesic effect of the caudalblock was evaluated using the Children's Hospital of EasternOntario Pain Scale (CHEOPS) and sedation was assessed usingthe Steward score at 30 min after extubation and at 1, 2, 4,6, 12 and 24 h. The first analgesic requirement time and side-effectsin a 24 h period were also recorded. Results. There were no differences in characteristics betweenthe groups. The end-tidal concentration of sevoflurane at extubationin Group F was significantly lower than in Group S. However,there was no significant difference in time from discontinuationof the volatile anaesthetics to tracheal extubation. No statisticaldifferences were found in the CHEOPS and Steward score, andthe time to first analgesia. The incidence of postoperativevomiting was not significantly different. Conclusion. We found that the addition of fentanyl 1 µgkg^–1 to ropivacaine 0.2% for caudal analgesia providesno further analgesic advantages over ropivacaine 0.2% alone.     

曲马多对异氟醚的MAC和循环的影响

观察４１例患者应用曲马多后对异氟醚ＭＡＣ的影响及对血液动力学的影响。静滴曲马多２ｍｇ／ｋｇ，在３１～５５岁组和≥５６岁组患者的异氟酸ＭＡＣ值分别为１.０７％和０.９６％，静滴曲马多４ｍｇ／ｋｇ，在这两个年龄组异氟醚ＭＡＣ值分别为０．９８％和０．９０％。和基础值相比，静滴由马多４ｍｇ／ｋｇ后患者心率和血压分别增加 ２３． ５％（Ｐ＜０． ００１）和 ７． ７％（Ｐ＜０． ００１）， １０分钟后 Ⅱ组患者的心率和血压均显著高于Ⅰ组（Ｐ<０．０２和０．００２）。结果表明，曲马多可强化吸入麻醉药，大剂量时还有明显的循环效应。     

犬静脉注射乳化异氟醚最低肺泡有效浓度的研究

目的测定犬静脉注射乳化异氟醚的最低肺泡有效浓度(MAC静脉),并与吸入异氟醚麻醉时的最低肺泡有效浓度(MAC吸入)进行比较。方法将40只杂种犬平均分成静脉和吸入麻醉两组。应用序贯法和自身交叉法同时测定犬的MAC值。结果静脉组序贯法所测得的MAC静脉(0.94±0.10)%,与自身交叉法所测得的前6个交叉点的MAC静脉(0.89±0.14)%或全部交叉点的MAC静脉(0.93±0.13)%之间差异均无显著意义(P>0.05)。吸入组序贯法所测得的MAC吸入(1.29±0.10)%,与自身交叉法所测得的前6个交叉点的MAC吸入(1.24±0.06)%或全部交叉点的MAC吸入(1.33±0.09)%之间差异亦无显著意义(P>0.05)。但两组间比较MAC静脉均小于MAC吸入,差异有显著意义(P<0.05)。结论乳化异氟醚静脉麻醉时的MAC静脉明显小于吸入异氟醚麻醉时的MAC吸入,序贯法和自身交叉法对MAC的测定结果无明显影响。     

Questioning the cardiocirculatory excitatory effects of opioids under volatile anaesthesia

Background. Opioid-induced hyperalgesia has been demonstratedin awake animals. We observed an increased haemodynamic reactivityin response to noxious stimuli in rats under sevoflurane anaesthesiatreated with a very low dose of sufentanil. The aim of thisinvestigation was to determine whether the two phenomena sharea common origin: an opioid-induced excitatory reaction. To addressthis, we administered several drugs with proven efficacy inopioid hyperalgesia to rats presenting with haemodynamic hyper-reactivity. Methods. The MACbar of sevoflurane was measured in controlsand in animals treated with sufentanil 0.005 µg kg^–1min^–1 before and after administration of i.v. (0.25, 0.5mg kg^–1) and intrathecal (i.t.) (250 µg) ketamine,i.v. (0.5, 1 mg kg^–1) and i.t. (30 µg) MK-801(NMDAantagonist), i.v. (0.1, 0.5 mg kg^–1) naloxone, i.v. (10mg kg^–1) and i.t. (50, 100 µg) ketorolac or i.t.(100, 150 µg) meloxicam (COX-2 inhibitor). Results. Sufentanil 0.005 µg kg^–1 min^–1 significantlyincreased MACbar (3.2 (SD 0.3) versus 1.9 (0.3) vol%). Withthe exception of naloxone, all drugs displayed a significantMACbar-sparing effect (>50%) in controls. Naloxone completelyprevented haemodynamic hyperactivity. Two patterns of reactionwere recorded for the other drugs: either hyper-reactivity wassuppressed and the MACbar-sparing effect was maintained (i.t.ketamine, i.t. MK-801, i.t. ketorolac [100 µg], i.t. meloxicam[150 µg]) or hyper-reactivity was blocked but MACbar-sparingeffect was lost (i.v. ketamine [0.5 mg kg^–1], i.v. MK-801[0.5, 1 mg kg^–1], i.v. ketorolac [10 µg kg^–1],i.t. ketorolac [50 µg], i.t. meloxicam [100 µg]). Conclusions. We have demonstrated that low-dose sufentanil-inducedhaemodynamic hyper-reactivity is an excitatory µ-opiate-relatedphenomenon. This effect is reversed by drugs effective in treatingopiate-induced hyperalgesia.