Minimum alveolar concentration (MAC) of xenon with sevoflurane in humans

BACKGROUND: Although more than 30 yr ago the minimum alveolar concentration (MAC) of xenon was determined to be 71%, that previous study had technological limitations, and no other studies have confirmed the MAC value of xenon since. The current study was designed to confirm the MAC value of xenon in adult surgical patients using more modern techniques. METHODS: Sixty patients were anesthetized with sevoflurane with or without xenon. They were randomly allocated to one of four groups; patients in group 1 received no xenon, whereas those in groups 2, 3, and 4 received end-tidal concentrations of 20, 40, and 60%, respectively (n = 15 each group). Target end-tidal sevoflurane concentrations were chosen using the "up-and-down" method in each group. After steady state sevoflurane and xenon concentrations were maintained for at least 15 min, each patient was monitored for a somatic response at surgical incision. Somatic response was defined as any purposeful bodily movement. The MAC of sevoflurane and its reduction by xenon was evaluated using the multiple independent variable logistic regression model. RESULTS: The interaction coefficient of the multiple variable logistic regression was not significantly different from zero (P = 0.143). The MAC of xenon calculated as xenon concentration that would reduce MAC of sevoflurane to 0% was 63.1%. CONCLUSIONS: The authors could not determine whether interaction in blocking somatic responses in 50% of patients is additive. The MAC of xenon is in the range of the values that were predicted in a previous study.     

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.     

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.     

Sevoflurane preconditioning at 1 MAC only provides limited protection in patients undergoing coronary artery bypass surgery: a randomized bi-centre trial

BACKGROUND: Volatile agents can mimic ischaemic preconditioning leading to a decrease in myocardial infarct size. The present study investigated if a 15 min sevoflurane administration before cardiopulmonary bypass (CPB) has a cardioprotective effect in patients undergoing coronary surgery. METHODS: Seventy-two patients were randomized in two centres. The intervention group (S) received 1 MAC sevoflurane administrated via the ventilator for 15 min followed by a 15 min washout before CPB, the control group did not. The primary outcome was the postoperative troponin Ic peak. A biopsy of the atrium was taken during canulation for enzyme dosages. Results are expressed as mean (SD). RESULTS: Neither troponin Ic nor tissular enzyme measurement exhibited any difference between the groups: peak of troponin Ic was 4.4 (5.6) in S group vs 5.2 (6.6) ng ml(-1) in control group (ns). Intratissular ecto-5'-nucleotidase activity was 7.1 (4.3) vs 8.5 (11.9), protein kinase C activity was 27.1 (15.7) vs 29.2 (28.7), tyrosine kinase activity was 101 (54.1) vs 98.5 (63.3), and P38 MAPKinase activity was 131.1 (76.1) vs 127.1 (86.8) nmol mg protein(-1) min(-1) in S group and control group, respectively (ns). However there were fewer patients with low postoperative cardiac index in S group (11% in S vs 35% in control group, P < 0.05) when considering the per protocol population. In S group, 25% of patients required an inotropic support during the postoperative period, vs 36% of patients in control group (ns). CONCLUSIONS: This study did not show a significant preconditioning signal after 15 min of sevoflurane administration. The 15 min duration might be too short or the concentration of sevoflurane too low to induce cardioprotection detected by troponin I levels.     

Effect of two anaesthetic regimens on airway nitric oxide production in horses

There is evidence that halothane inhibits nitric oxide synthasein vitro, but the effect of intravenous anaesthetic agents isless clear. This study was undertaken to compare the rate ofexhaled nitric oxide production (V_NO) in spontaneously breathinghorses anaesthetized with halothane or an intravenous regimen.Seven adult horses were studied twice in random order. Afterpremedication with romifidine 100 µg kg^–1,anaesthesia was induced with ketamine 2.2 mg kg^–1and maintained with halothane in oxygen (HA) or by an intravenousinfusion of ketamine, guaiphenesin and romifidine (IV). Inhaledand exhaled nitric oxide (NO) concentrations, respiratory minuteventilation (V_E), pulmonary artery pressure (P_PA), fractionalinspired oxygen concentration (FI_O2), end-tidal carbon dioxideconcentration (E'_CO2), cardiac output (Q) and partial pressuresof oxygen and carbon dioxide in arterial blood (Pa_O2, Pa_CO2)were measured. Exhaled nitric oxide production rate was significantlylower (40 min, P<0.01; 60 min, P<0.02) duringHA [40 min, 1.4 (SD 1.4) pmol l^–1 kg^–1 min^–1;60 min, 0.7 (0.7) pmol l^–1 kg^–1 min^–1]than during IV [40 min, 9.3 (9.9) pmol l^–1 kg^–1min^–1; 60 min, 12.5 (13.3) pmol l^–1 kg^–1min^–1). Mean pulmonary artery pressure was significantlyhigher (40 min, P<0.01; 60 min, P<0.001) during HA[40 min, 5.9 (1.1) kPa; 60 min, 5.9 (0.9) kPa] comparedwith IV (40 min, 4.4 (0.4) kPa; 60 min, 4.4 (0.5) kPa].NO is reduced in the exhalate of horses anaesthetized with halothanecompared with an intravenous regimen. It is suggested that increasedmean pulmonary artery pressure during halothane anaesthesiamay be linked to the differences in NO production. Br J Anaesth 2001; 86: 127–30     

Minimum alveolar concentrations (MAC) of halothane and nitrous oxide in swine

To compare anesthetic effects using a swine model, we needed to know the minimum alveolar concentrations (MAC) of halothane and nitrous oxide that produce anesthesia in the pig. This information does not exist in literature. Furthermore, MAC varies considerably among species: by more than 60% for halothane, and by more than 200% for nitrous oxide. Therefore, using eight young swine, we determined mean (+/- SEM) MAC values for halothane (1.25 +/- 0.04% of one atmosphere) and nitrous oxide (277 +/- 18% of one atmosphere). These values are higher than values reported for other mammals. Factors possibly accounting for this variability include interspecies differences, age, body temperature, increased sympathetic activity, and differences in methodology.     

Emergence and early cognitive function in the elderly after xenon or desflurane anaesthesia: a double-blinded randomized controlled trial

Background: Postoperative cognitive impairment after general anaesthesia,especially in the elderly, is a well-recognized problem. Xenon,known to be an N-methyl-D-aspartate antagonist, may be advantageous.In this study, the early cognitive function in the elderly aftergeneral anaesthesia with xenon was compared with that afterdesflurane. Methods: After approval by the local ethical committee and after obtainingwritten informed consent, patients were enrolled in this randomized,double-blinded, controlled study. Thirty-eight patients (65–75yr old, ASA status I–III) undergoing an elective surgerywith a planned duration of 60–180 min were allocated toeither the xenon (n = 18) or the desflurane (n = 20) anaesthesiagroup. The primary outcome was the cognitive Test for AttentionalPerformance (TAP) with its subtests Alertness, Divided Attention,and Working Memory. After baseline assessment 12–24 hbefore operation, patients were followed-up 6–12 and 66–72h after operation. Secondary outcomes were emergence times fromanaesthesia and the modified Aldrete score. Results: No difference was found between the groups in the TAP at 6–12and 66–72 h after operation. In the xenon group, emergencetime was significantly faster for the following parameters:time to open eyes (P = 0.001), to react on demand (P = 0.001),to extubation (P = 0.001), and for time and spatial orientation(P = 0.007). The modified Aldrete score was significantly higherafter 30, 45 and 60 min in the xenon group. Conclusions: There was no difference in the postoperative cognitive testingat 6–12 and 66–72 h. Xenon was associated in theelderly with a faster emergence from general anaesthesia thandesflurane.     

Determination of sevoflurane alveolar concentration for tracheal intubation with remifentanil, and no muscle relaxant

The sevoflurane alveolar concentration needed for tracheal intubation with remifentanil was studied in 26 adult patients premedicated with 100 mg hydroxyzine. Anaesthesia was induced with sevoflurane in oxygen. The concentration was determined by Dixon's up-and-down method. The first patient was tested at 4.5%. One minute after obtaining the preselected value, remifentanil 1 microg.kg-1 was injected for 60 s followed by an infusion of 0.25 microg.kg-1. min-1. Ventilation was then manually assisted for 2 min and tracheal intubation was attempted. Tracheal intubation conditions and responses to intubation were noted. Heart rate and mean arterial pressure were recorded before induction, before remifentanil injection, and before and 3 min after tracheal intubation. The concentration for acceptable intubating conditions was 2.5 +/- 0.7%. From logistic regression, ED50 and ED95 were 2.0% (95% CI 1.3-2.5) and 3.2% (95% CI 2.6-5.6), respectively. With sevoflurane 2.5%, heart rate and mean arterial pressure decreased by 18% and 15%, respectively, after remifentanil administration and increased slightly after tracheal intubation.     

Prospective comparison of sevoflurane and desflurane in formerly premature infants undergoing inguinal herniotomy

Background. Formerly premature infants having inguinal herniotomyhave been at a high risk of postoperative apnoea, newer lesssoluble anaesthetic agents may reduce this risk. Methods. Thirty infants, under 37 weeks gestation and under47 weeks post-conceptional age, undergoing inguinal herniotomyhad an inhalational induction with sevoflurane and were randomlyallocated to sevoflurane (group S) or desflurane (group D) formaintenance. All infants received i.v. atracurium 0.5 mg kg^–1,rectal acetaminophen 20 mg kg^–1 and caudal bupivacaine0.25% 1 ml kg^–1. Infants were monitored for apnoeas (usingnasal thermistry and impedance), haemoglobin oxygen desaturationsand bradycardias for 12 h before and after operation with anAlice^® 4 polysomnograph. Emergence timings were recorded. Results. There was no difference between pre- and postoperativeincidence of apnoeas in either group, and no group differencebetween desflurane and sevoflurane in terms of pre- and postoperativeventilatory events or in the number of apnoeas in the postoperativeperiod (nine patients in group D and five patients in groupS had apnoeas). Median times to first movement, tracheal extubation,eye opening and first cry were all faster with group D (groupD: 3.0, 10.0, 9.0 and 11.0 min and group S: 7.0, 15.1, 13.5and 16.1 min, respectively). No infant had problems with airwayirritation on emergence and no infant required airway interventionfor apnoea. Conclusions. Infants wake faster from general anaesthesia whenmaintained with desflurane as compared with sevoflurane, butno difference in postoperative respiratory events was demonstratedbetween the groups.     

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     

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     

Nomogram to estimate age-related MAC

Background. In clinical practice it is difficult to estimaterapidly two important values: (i) the total age-corrected MACmultiple from measured end-expired concentrations of volatileagent and nitrous oxide; (ii) the end-expired concentrationof volatile agent needed to obtain a given total MAC multiple.We have developed a nomogram to do this. Methods. We used standard nomogram methods to construct onesingle nomogram covering wide ranges of age (1–100 yr)and MAC (0.1–1.8 MAC) for halothane, enflurane, isoflurane,sevoflurane, and desflurane, alone or in combination with variousconcentrations of nitrous oxide. The user only has to draw twostraight lines to obtain the desired result. Results. The nomogram is simple to use. End-expired concentrationsof halothane 0.48%, enflurane 1.05%, isoflurane 0.75%, sevoflurane1.18%, or desflurane 4.3% in the presence of nitrous oxide 50%will give 1.4 MAC in a patient of 75 yr vs 0.9 MAC in a 1-yr-old.A reverse example is: a total MAC of 1.3 when using sevofluraneand nitrous oxide 67% in oxygen, requires an end-expired sevofluraneconcentration of 1.8% in a 3-yr-old whereas 0.55% is neededin a patient of 90 yr. Conclusions. The nomogram gives accurate results if it coversa whole A4 sheet in landscape format and could be extended toapply to other agents, for example xenon.     

Emergence and recovery in children after desflurane and isoflurane anaesthesia: effect of anaesthetic duration

Background. We hypothesized that increasing duration of inhalationanaesthesia is associated with slower emergence and recoveryin children, and that this effect would be less marked withdesflurane in comparison with isoflurane. Methods. Fifty-four infants and children assigned in groupsaccording to age and expected length of operation were prospectivelyrandomized to receive either isoflurane (I) or desflurane (D)for anaesthesia. After standard induction, the anaesthesia wasmaintained using an age-related 1.0 minimum alveolar concentration(MAC) equivalent for either agent in air and oxygen. Local analgesiawas used as appropriate. End-tidal volatile agent concentrationwas recorded until extubation. Clinical evaluation of recoverywas made by observers, blinded to group allocation. Results. For patients <4 yr of age, the median (95% CI) timesin minutes to first movement [5.27 (D), 9.22 (I)], eye opening[9.42(D), 13.3(I)] and extubation [7.18 (D), 12.5 (I)] weresignificantly shorter (P<0.05) for desflurane. In the group>4 yr of age, the median (95% CI) times in minutes to firstmovement [4.42 (D), 11.6 (I)], eye opening [8.55(D), 18.0(I)]and extubation [7.08 (D), 16.7 (I)] were significantly shorter(P<0.001) for desflurane. Times to leave recovery were notsignificantly different for the group <4 yr of age, but weresignificantly shorter for desflurane in the group >4 yr ofage (P<0.01). The isoflurane, but not desflurane, had a time-dependenteffect on arousal. There were no significant differences inincidence of airway irritation or emergence delirium betweenthe two agents. Conclusions. The rate of recovery in children after exposureto desflurane was faster than those patients receiving isoflurane;recovery from desflurane, but not isoflurane, was relativelyunaffected by the duration of anaesthesia.     

Phenotyping malignant hyperthermia susceptibility by measuring halothane-induced changes in myoplasmic calcium concentration in cultured human skeletal muscle cells

Background. Malignant hyperthermia (MH) is a potentially lethaldisease triggered by volatile anaesthetics and succinylcholinein genetically predisposed individuals. Because of the heterogeneticnature of MH, a simple genetic-based diagnostic test is notfeasible and diagnosis requires an invasive open muscle biopsyfollowed by the in vitro contracture test (IVCT). Our aim wasto establish if measurements of halothane-induced increasesin intracellular calcium ion concentration [Ca²⁺]_i in culturedhuman skeletal muscle cells can be used to phenotype MH susceptibilityand if different mutations in the ryanodine receptor (RYR1)gene affect halothane-induced increases in [Ca²⁺]_i. Methods. Primary cultures of human skeletal muscle cells wereestablished from 54 individuals diagnosed by the IVCT accordingto the protocol of the European MH Group as: MH susceptible(n=22), MH negative (n=18) or MH equivocal (n=14). All individualswere screened for the presence of the most common mutationsin the RYR1 gene. [Ca²⁺]_i was measured by fluorescent digitalmicroscopy using fura-2/AM in 10 cells from each patient atfive different halothane concentrations. Results. The halothane-induced increase in [Ca²⁺]_i differedsignificantly between the three diagnostic groups. Differentmutations of the RYR1 gene did not have a specific impact onhalothane-induced increases in [Ca²⁺]_i. Conclusions. Measurements of [Ca²⁺]_i in human skeletal musclecells can be used to phenotype MH susceptibility; however, wedid not observe a specific effect of any mutation in the RYR1gene on the halothane-induced increase in [Ca²⁺]_i. Br J Anaesth 2002; 89: 571–9     

Minimum alveolar concentration of halothanediethyl-ether azeotrope

The azeotropic mixture of halothane and diethyl ether (HE) may be a valuable alternative to other anaesthetic agents under circumstances such as war, civil disaster, and primitive conditions. In the present study the minimum alveolar concentrations (MACs) for HE in man (n = 25) and in pigs (n = 6) were determined. For comparison with results of other studies, the MAC for halothane in man (n = 14) was also determined. A Normac gas analyser and a Varian 3700 gas chromatograph were calibrated against known standards of HE. The performance of two vaporizers (Fluotec Mark III, Servo vaporizer for halothane) was studied. The Fluotec Mark III vaporizer and the Servo halothane vaporizer filled with HE gave a linear performance with increasing dial settings. The Normac gas analyser set for methoxyflurane was linearly sensitive to the ether component of the azeotrope. The MAC for HE in man was 0.71 vol.% +/- 0.03 (s.e.mean) (ether 0.21 vol.%, halothane 0.50 vol.%) in the age group 19-42 years. MAC for halothane in man was 0.65 +/- 0.03 in the age group 19-32 years. The MAC for HE in pigs between 20-24 kg was 0.99 vol.% +/- 0.07. The ether component seems to act synergistically with halothane in the azeotropic mixture. The present study provides an opportunity to compare HE with other volatile anaesthetic agents.     

Minimum anesthetic concentration of sevoflurane with different xenon concentrations in swine

In a previous study, we described a partial antagonism of xenon (Xe) in combination with isoflurane. One hypothetical explanation suggested that Xe and isoflurane probably induced anesthesia via different pathways at the neuronal level. This warranted investigating the combination of Xe with other inhaled anesthetics to examine the relationship between Xe and volatile anesthetics in general. We therefore investigated the influence of Xe on the minimum alveolar concentration (MAC) of sevoflurane. The study was performed in 10 swine (weight 30.8 kg +/- 2.6, mean +/- SD) ventilated with xenon 0%, 15%, 30%, 40%, 50%, and 65% in oxygen. At each Xe concentration, various concentrations of sevoflurane were administered in a stepwise design. For each a supramaximal pain stimulus (claw clamp) was applied. The appearance of a withdrawal reaction was recorded. The sevoflurane MAC was defined as the end-tidal concentration required to produce a 50% response rate. At each Xe concentration, the animals' responses to the pain stimulus were categorized and a logistic regression model was fitted to the results to determine sevoflurane MAC. Sevoflurane MAC was decreased by inhalation of Xe in a linear manner from 2.53 with 0% Xe to 1.54 with 65% Xe. In contrast to Xe and isoflurane, the anesthetic effects of Xe and sevoflurane appear to be simply linear. IMPLICATIONS: We investigated the influence of the anesthetic gas, xenon, on the minimum alveolar concentration (MAC) for the volatile anesthetic sevoflurane. The study was performed in 10 swine ventilated with fixed xenon and various concentrations of isoflurane. The sevoflurane MAC is decreased by inhalation of xenon in a linear relationship.     

新生儿七氟烷最低肺泡有效浓度

目的 确定新生儿七氟烷的最低肺泡有效浓度(MAC).方法 择期全麻新生儿30例,正常体重,ASA分级Ⅰ或Ⅱ级.吸入6.00％七氟烷诱导气管插管,机械通气后调整吸入七氟烷浓度以达到呼气末浓度的预定值,维持20 min后开始切皮.根据改良序贯法进行试验,初始七氟烷呼气末浓度为3.00％,切皮时发生体动反应,下一例升高一个浓度梯度,切皮时未发生体动反应,下一例降低一个浓度梯度,相邻浓度梯度为0.25％.采用逻辑回归法计算新生儿七氟烷MAC和95％有效浓度及其95％可信区间.结果 新生儿七氟烷MAC和95％有效浓度及其95％可信区间分别为2.82％(2.66％ ～ 2.98％)和3.39％(2.89％～3.89％).结论 国内新生儿七氟烷MAC为2.82％,低于目前国外参考值.     

The effects of i.v. fentanyl administration on the minimum alveolar concentration of isoflurane in horses

Background. Fentanyl decreases the minimum alveolar concentration(MAC) of inhaled anaesthetics and has been used clinically toreduce the requirements of other anaesthetic drugs in humansand small animals. We hypothesized that i.v. fentanyl woulddecrease the MAC of isoflurane in horses in a dose-dependentmanner. Methods. Following determination of baseline MAC of isoflurane,fentanyl was administered i.v. to target plasma concentrationsof 1, 8 and 16 ng ml^–1. Each horse was randomly assignedtwo of three target concentrations administered in ascendingorder. Loading and infusion doses for each horse were determinedfrom previously derived individual pharmacokinetic values. IsofluraneMAC determination began 45 min after fentanyl administrationat each target fentanyl concentration. Venous blood was collectedat fixed intervals during the infusion for measurement of plasmafentanyl concentrations. Results. Mean actual fentanyl plasma concentrations were 0 (baseline),and 0.72 (SD 0.26), 8.43 (3.22), and 13.31 (6.66) ng ml^–1for the target concentrations of 1, 8 and 16 ng ml^–1,respectively. The corresponding isoflurane MAC values were abaseline of 1.57 (0.23), and 1.51 (0.24), 1.41 (0.23) and 1.37(0.09)%, respectively. The fentanyl concentrations of 0.72 and8.43 ng ml^–1 did not significantly alter the MAC of isoflurane,but an 18 (7)% ISO-MAC reduction was observed at the 13.31 ngml^–1 concentration. Conclusions. These results cautiously encourage further studyof fentanyl as an opioid anaesthetic adjunct to inhalant anaesthesiain horses.     

Effects of xenon anaesthesia on intestinal oxygenation in acutely instrumented pigs

Background. Xenon is a narcotic gas that might be able to replacevolatile anaesthetics or nitrous oxide due to its favourablepharmacological properties, such as providing haemodynamic stability.Intestinal oxygenation is affected by most volatile anaestheticsas a result of cardiodepressive effects. Reducing oxygenationof the gut might be a factor leading to perioperative organdysfunction. This animal study was designed to assess the effectsof xenon on intestinal oxygenation. Methods. After ethical approval, 24 anaesthetized, acutely instrumentedpigs were randomly assigned to three groups: nine animals receivedxenon anaesthesia with inspiratory concentrations of 0, 20,50 and 65% in addition to their basic i.v. anaesthesia, nineanimals served as a study control group, and five animals wereused to assess model stability. Measurement of systemic andregional haemodynamic and oxygenation parameters was made 30min after changing the xenon concentration. Results. Xenon elicited dose-dependent systemic haemodynamicchanges: heart rate and cardiac output decreased by 30%, whilemean arterial pressure was stable. Superior mesenteric arteryblood flow was lower in the xenon group. Vascular resistanceof the superior mesenteric artery increased. The small intestinaloxygen supply decreased with increasing xenon concentration;the mucosal tissue oxygen partial pressure decreased but didnot reach hypoxic (<5 mm Hg) values. Serosal tissue oxygenpartial pressure was maintained. Conclusions. Xenon, in addition to basic i.v. anaesthesia, eliciteda decrease in cardiac output and maintained mean arterial pressure.Intestinal oxygenation was maintained, although regional macrohaemodynamicperfusion decreased. Xenon does not impair intestinal oxygenationunder physiological conditions.