End-tidal Enflurane Concentration Research Articles

Caudal anesthesia reduces the minimum alveolar concentration of enflurane for laryngeal mask airway removal in boys

To investigate the effects of caudal analgesia on the minimal alveolar concentration of enflurane for laryngeal mask airway (LMA) smooth extubation (MACex). We studied 50 nonpremedicated children, aged three to ten years, ASA physical status I, undergoing surgery for hypospadias repair. After a sevoflurane inhalation induction, children were randomized to receive LMA insertion with or without ropivacaine caudal analgesia. At the end of surgery, a predetermined end-tidal enflurane concentration was achieved, and the LMA was removed by an anesthesiologist blinded to group allocation. Each concentration at which LMA extubation was attempted was predetermined by the up-and-down method (with 0.1% as the step size). When LMA removal was accomplished without coughing, clenching teeth or gross purposeful muscular movements during or within one minute after removal, it was considered successful. MACex of enflurane for LMA removal in the group without caudal anesthesia was 1.04% (95% confidence interval, 1.00-1.10) and the LMA MACex of enflurane in the group with caudal anesthesia was 0.74% (95% confidence interval, 0.63-0.81). Caudal analgesia significantly reduced enflurane requirements by 29% (95% confidence interval, 22-36%). In conclusion, caudal analgesia significantly reduced the LMA MACex of enflurane by approximately 29%. Possible mechanisms may be related to the analgesic effect of caudal blockade or to the sedative properties of neuraxial anesthesia.

The Effect of Anesthetics on Somatosensorily Evoked Potentials during Surgery

Background : Many methods are available for the monitoring of spinal cord injury during an operation. During anesthesia, somatosensily evoked potentials (SSEP) may undergo substantial changes in the latencies and amplitudes which may be interpreted as pathological. It is essential for the anesthesiologist to know the potential interactions between anesthetic drugs and neurophysiologic responses during operation. The depressant effect of inhalation agents on the central nervous system exceeds commonly used intravenous anesthetics. Therefore, intravenous anesthesia is preferred to inhalation agents. This study was designed to compare the effects of intravenous anesthetics (propofol and fentanyl) and inhalational anesthetics (enflurane and nitrous oxide) used in the operation room. Methods : According to the inclusion criteria of ASA I-II, 40 patients who were free of neurologic disease with electric abdominal operations were randomly selected. The baseline of the SSEPs were recorded with stimulation of the posterior tibial nerve at the ankle. After obtaining the baseline (preinduction) of the SSEPs, intravenous anesthetics (propofol 10 mg/kg/h, fentanyl 1 2 μg/kg) and inhalational anesthetics (end tidal enflurane concentration 1.0 vol %, 50% nitrous oxide in oxygen) were administered. 30 minutes after induction (steady state), additional SSEPs were recorded. Mean arterial pressure, heart rate, temperature and arterial blood carbon dioxide tension were monitored. Results : There were no significant differences in the baseline of SSEPs between the intravenous anesthetics group and the inhalational anesthetics group. There were no significant differences in latencies and amplitudes between the preanesthesia state and the postanesthetia state in the intravenous anesthetics group. But the inhalational anesthetics group revealed prolonged latencies in the postanestesia state as compared with their preanesthesia state. Conclusions : The above findings suggest that the use of intravenous anesthetics can be beneficial to intraoperative SSEP monitoring for possible damage to the central nervous system during operations. (Korean J Anesthesiol 1999; 37: 368∼374)

Tramadol or morphine administered during operation: a study of immediate postoperative effects after abdominal hysterectomy

Tramadol may cause awareness and EEG activation during anaesthesia. We compared tramadol with morphine, administered during wound-closure, surmising that tramadol may cause earlier awakening, more rapid recovery, less respiratory depression and equivalent pain relief. Forty patients received nitrous oxide-enflurane for abdominal surgery. At wound closure, patients received tramadol 3 mg kg-1 or morphine 0.2 mg kg-1 and end-tidal enflurane concentrations were maintained at 0.5 kPa until skin closure, whereupon anaesthesia was discontinued. Times to spontaneous respiration, awakening and orientation were similar in the two groups, as were blood-gas tensions, ventilatory frequency, pain scores and incidence of nausea. Half of each group required supplementary analgesia during their 90-min stay in the recovery room. P-deletion counts improved more rapidly in the tramadol group. This study confirms previous reports that tramadol did not antagonize the hypnotic effects of volatile anaesthetics. Tramadol, administered during operation, was as effective as morphine in providing postoperative analgesia while permitting more rapid psychomotor recovery.

Dependence of the Adequacy of Muscle Relaxation on the Degree of Neuromuscular Block and Depth of Enflurane Anesthesia During Abdominal Surgery

We studied the intensity of neuromuscular block that is adequate for surgical relaxation at different end-tidal levels of enflurane during N2 O-O2-fentanyl anesthesia in 30 patients undergoing upper abdominal surgery. After induction of anesthesia with thiopental 4-6 mg/kg and vecuronium 0.07 mg/kg intravenously (I.V.), patients were randomly assigned to receive nitrous oxide-oxygen (2:1) and enflurane at 0.3% (Group I), 0.6% (Group II), or 1.2% (Group III) end-tidal level throughout anesthesia. The initial neuromuscular block was allowed to terminate and additional increments of 1 mg vecuronium were given when indicated by clinical signs or by spontaneous electromyography of neck muscles. In Group I additional vecuronium had to be given 62 times and in Groups II and III, 33, and 16 times, respectively. The mean (SD) neuromuscular block at the time of additional vecuronium was 75.9% +/- 20.7%, 62.5% +/- 20.1%, and 39.3% +/- 21.1% in Groups I to III, respectively. We conclude that there was a clear linear relationship between the end-tidal concentration of enflurane and the degree of neuromuscular block necessary to produce adequate surgical muscle relaxation (P < 0.001). (Anesth Analg 1995;80:543-7)

Effect of low-dose enflurane on the ventilatory response to hypoxia in humans

To investigate the effects of enflurane on the control of breathing we have studied the ventilatory responses to isocapnic hypoxia in 12 adults with and without sedation with enflurane. Design 1 consisted of three steps into hypoxia (PE' O2 = 6.7 kPa), each lasting 3 min, separated by periods of euoxia lasting 5 min (PE' O2 = 13.3 kPa). Design 1 was repeated four times in each subject on the same day in random order: with carrier gas (control) and with 0.04 MAC, 0.07 MAC and 0.13 MAC of end-tidal enflurane concentrations. Design 2 consisted of 20-min exposures to hypoxia with and without 0.07 MAC of enflurane. Each exposure was preceded and followed by 5 min of euoxia. End-tidal PCO2 was held constant at 0.13-0.27 kPa greater than the resting level throughout both designs. Mean (SEM) ventilatory responses to hypoxia for design 1 were: 8.2 (1.3) litre min-1 (control), 6.6 (1.4) litre min-1 (0.04 MAC), 5.7 (1.1) litre min-1 (0.07 MAC) and 3.7 (0.5) litre min-1 (0.13 MAC) (P < 0.001). For design 2, enflurane produced a 15% reduction in resting ventilation (P < 0.01), a 40% decrease in the acute ventilatory response to hypoxia (P < 0.01) and a 32% reduction in ventilatory decline (ns) which occurred during sustained hypoxia.

Clinical enflurane metabolism by cytochrome P450 2E1

Fluorinated ether anesthetic hepatotoxicity and nephrotoxicity are mediated by cytochrome P450-catalyzed oxidative metabolism. Metabolism of the volatile anesthetic enflurane to inorganic fluoride ion by human liver microsomes in vitro is catalyzed predominantly by the cytochrome P450 isoform CYP2E1. This investigation tested the hypothesis that P450 2E1 is also the isoform responsible for human enflurane metabolism in vivo. Disulfiram, which is converted in vivo to a selective inhibitor of P450 2E1, was used as a metabolic probe for P450 2E1. Twenty patients undergoing elective surgery were randomized to receive disulfiram (500 mg orally; n = 10) or nothing (control subjects; n = 10) the evening before surgery. All patients received a standard anesthetic of enflurane (2.2% end-tidal) in oxygen for 3 hours. Blood enflurane concentrations were measured by gas chromatography. Plasma and urine fluoride concentrations were quantitated by ion-selective electrode. Patient groups were similar with respect to age, weight, gender, duration of surgery, and blood loss. Total enflurane dose, measured by cumulative end-tidal enflurane concentrations (3.9 to 4.1 MAC-hr) and by blood enflurane concentrations, was similar in both groups. Plasma fluoride concentrations increased from 3.6 +/- 1.5 mumol/L (baseline) to 24.3 +/- 3.8 mumol/L (peak) in untreated patients (mean +/- SE). Disulfiram treatment completely abolished the rise in plasma fluoride concentration. Urine fluoride excretion was similarly significantly diminished in disulfiram-treated patients. Fluoride excretion in disulfiram-treated patients was 62 +/- 10 and 61 +/- 12 mumol on days 1 and 2, respectively, compared with 1090 +/- 180 and 1200 +/- 220 mumol in control subjects (p < 0.05 on each day). Disulfiram prevented fluoride ion production after enflurane anesthesia. These results suggest that P450 2E1 is the predominant P450 isoform responsible for human clinical enflurane metabolism in vivo.

Intrathecal morphine during thoracotomy, part 1: Effect on intraoperative enflurane requirements

The ability of intrathecal morphine to reduce the anesthetic requirements during thoracotomy was investigated. Twenty-four patients scheduled for thoracic surgery were studied. Anesthesia was induced with thiamylal sodium, 4 mg/kg, fentanyl, 100 μg, and 100 mg of succinylcholine. Prior to skin incision, 12 patients received intrathecal injection of 12 μg/kg of preservative-free morphine sulfate (ITM), while the remaining 12 patients served as controls. The ITM was given undiluted at the L3–4 or L4–5 level. Anesthesia was maintained solely with enflurane, titrated to keep mean arterial pressure within 15% of the preoperative values. Vecuronium was given as required for relaxation. No additional narcotics were administered. Throughout the procedure, end-tidal (ET) enflurane concentration was recorded at 15-minute intervals from the mass spectrometer (Perkin Elmer). The intraoperative mean ET concentration of enflurane was significantly reduced in the ITM group beginning 1 hour after the injection (1.19 ± .45% in the control group versus 0.73 ± 0.08% in the ITM group). The enflurane requirements, expressed as percent end-tidal enflurane/hour, were significantly less in the ITM group for the duration of the procedure (0.8 ± .17 v 1.08 ± .22, respectively). In conclusion, when administered prior to skin incision for post-thoracotomy pain control, intrathecal morphine reduces intraoperative enflurane requirements.

Does hypothermia or hyperventilation affect enflurane MAC reduction following partial cardiopulmonary bypass in dogs?

This study in dogs determined the effect of systemic cooling and arterial hypocarbia during cardiopulmonary bypass (CPB) on the requirements for enflurane anaesthesia (MAC) before and after CPB. Twelve mongrel dogs were each anaesthetized with enflurane in oxygen on two separate occasions. End-tidal enflurane concentration was measured with a Puritan-Bennett Anaesthesia Agent Monitor. Using the tail-clamp method, MAC was determined twice with a one-hour interval between measurements (MAC 1 and MAC 2). Partial CPB was then initiated using femoral arterio-venous cannulation and maintained for one hour. Following separation from CPB, MAC was again determined twice with a one hour interval between measurements (MAC 3 and MAC 4). Dogs were randomly assigned according to PaCO2 management during CPB (low, 17.6 +/- 8.6 mmHg vs high, 38.9 +/- 11.5 mmHg), and then subjected to two experimental conditions. The first experiment on each dog was undertaken using normothermia during CPB (warm, 35-37 degrees C) while the second experiment (at least two weeks later) was conducted using hypothermia during CPB (cold, 30 degrees C). Analysis of the data, using ANOVA for repeated measures, revealed MAC 3 (1.95 +/- 0.33%, post-CPB) to be reduced when compared with MAC 1 (2.18 +/- 0.28%, P < 0.01) or MAC 2 (2.10 +/- 0.22%, P < 0.01), determined before CPB. Multivariate repeated measures analysis revealed no independent effects of hypothermia or arterial hypocarbia during CPB, on MAC reduction. By the time of the second experiment in each dog (two weeks later), MAC had returned to baseline levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood/gas solubility coefficient and blood concentration of enflurane during normothermic and hypothermic cardiopulmonary bypass

The blood/gas solubility coefficient and blood concentration of enflurane were measured at intervals in 10 patients undergoing coronary artery revascularization with cardiopulmonary bypass (CPB) and moderate hypothermia. A constant end-tidal concentration of enflurane was maintained throughout the study. Blood/gas solubility coefficient was determined at 37°C, which when combined with an initial single-step equilibration of the blood sample with air, permitted the accurate measurement of blood concentration. Blood/gas solubility coefficient and blood concentration both decreased significantly with the onset of CPB. During the period of hypothermia, blood/gas solubility as measured at 37°C showed little change; however, there was a progressive, marked increase in blood concentration with a mean increase of 80% prior to rewarming. Therefore, the level of anesthesia provided by enflurane may lighten with the onset of CPB, and a deeper level will accompany any decrease in blood temperature. On rewarming, blood concentration levels rapidly returned to levels similar to those measured before cooling. The increased uptake and accumulation of volatile anesthetic agent that occurred as a result of the period of hypothermic CPB was rapidly cleared. The rapidity with which blood concentration responded to the changes occurring during CPB make it unlikely that there was any significant increase in myocardial depression in response to the raised blood concentration secondary to the hypothermia.

Does Cardiopulmonary Bypass Alter Enflurane Requirements for Anesthesia?

This study on dogs determined whether the requirement for enflurane anesthesia was different pre- versus postcardiopulmonary bypass (CPB). Male mongrel dogs (n = 16) were anesthetized with enflurane in oxygen. Tracheal intubation was performed, monitors placed, and end-tidal enflurane concentration measured via a Puritan-Bennett Anesthesia Agent Monitor. MAC was determined by the tail-clamp method. CPB was then initiated using aortoatrial (n = 6, group 1) or femoral artery-vein (n = 4, group 2) cannulation or none (n = 6, group 3, control). CPB was maintained for 1 h using a bubble oxygenator, a crystalloid prime, and flows of approximately 70-80 ml/kg with a mean systemic pressure maintained between 50-70 mmHg. Following separation from CPB, MAC was again determined. The reduction in enflurane MAC following CPB was 30.1 +/- 21.5% (mean +/- SD; P less than 0.05 vs. pre-CPB) in group 1 but there was a wide range of reduction produced (3.8-58.8%). The degree of MAC reduction (19.8 +/- 8.6%; P less than 0.05 vs. pre-CPB) produced by CPB in group 2 was much less variable in degree (range 13.0-32.4%) but did not differ from group 1. Although pre- versus post-CPB mean systemic pressure fell from 83 +/- 13 to 69 +/- 15 mmHg (P less than 0.05), this is above the level likely to produce a reduction in MAC. No other significant hemodynamic changes were observed. Temperature pre- versus post-CPB was not different. The degree of hemodilution and acid-base disturbances are unlikely to be the explanation.(ABSTRACT TRUNCATED AT 250 WORDS)

Dezocine-MAC Reduction and Evidence for Myocardial Depression in the Presence of Enflurane

The effect of dezocine, an agonist-antagonist opioid analgesic, on enflurane MAC (EMAC) was measured in dogs and, in a separate study, the hemodynamic effects of IV bolus doses of dezocine in the presence of a stable end-tidal enflurane concentration were measured. Study 1 (n = 8)--EMAC Reduction: Dezocine reduced EMAC in a dose-dependent fashion by a maximum of 58 +/- 3% (mean +/- SEM) after injection of 20 mg/kg. Cardiac toxicity prevented administration of higher doses. Study 2--Hemodynamics: Group 1 (n = 7) received dezocine 0.2, 1.5, 5, and 20 mg/kg IV each as a bolus over 30 sec. Group 2 (n = 5) was studied in exactly the same manner except that instead of dezocine, each dog received drug carrier solution alone (carrier). Significant hemodynamic differences between carrier and drug groups were observed only at the 20 mg/kg dose level, which produced death in one dog and a decrease in mean aortic pressure to 39 +/- 5% of baseline, in cardiac output to 60 +/- 9% of baseline, and in stroke volume to 69 +/- 9% of baseline in the remaining dogs. It is concluded that dezocine produces a dose-dependent reduction in EMAC limited by cardiovascular toxicity. This toxicity appears to be related to direct myocardial depression by high doses of dezocine in the presence of enflurane.

吸入麻酔薬（エンフルラン，ハロタン，笑気）の聴性脳幹反応（ＡＢＲ）に及ぼす影響

The effects of inhalation anesthetics (enflurane, halothane, nitrous oxide) and hyperventilation on brainstem auditory evoked responses (BAER) were studied in 52 patients underwent lower abdominal surgeries with spinal continuous peridural anesthesia, that was able to exclude noxious stimuli of the surgical procedures. Under normothermic, normocapnic and normotensive status, with increasing end-tidal concentration of enflurane and halothane, the interpeak latencies (IPL) I-II, III-V and I-V increased with a linear dose-related manner. While, with nitrous oxide (66%), IPL I-III increased, but IPL III-V didn't change. This results showed that enflurane and halothane influenced the auditory pathway from the acoustic nerve to the thalamus with a linear dose-related manner. However, nitrous oxide was different from halogenized agents, such as enflurane and halothane, in the effects on the brainstem. Under hyperventilation (PaCO2 30-25mmHg) with 1.0% enflurane, IPL I-V increased significantly in comparison with normoventilation (PaCO2 45-35mmHg). High concentratian of enflurane with hyperventilation should be given carefully, bacause BAER latency delay was considered to be related with seizure activity of enflurane.

Feedback Control of Enflurane Delivery in Dogs???Inspired Compared to End-Tidal Control

A technique was studied for the rapid induction of anesthesia in a closed rebreathing circuit using feedback control of end-tidal enflurane concentration. This technique was compared to anesthetic induction using a constant inspired concentration. In one group of seven dogs, end-tidal enflurane concentration was maintained at 2.0%. Electronic feedback control automatically decreased the inspired concentration from a maximum of 3.7% to 2.1% during a 4-hr period. In the second group of seven dogs, the inspired enflurane concentration was 2.0% throughout the study. There was no statistically significant difference between the two groups with regard to enflurane uptake, heart rate, blood pressure, or cardiac output. Enflurane uptake was higher in the first group only during the first 6 min after induction. The induction technique that used feedback control to automatically adjust the inspired enflurane concentration appeared to have no adverse cardiovascular effects beyond those present during an induction using a constant inspired concentration.

ENFLURANE ANAESTHESIA CAUSES GRADED CHANGES IN THE BRAINSTEM AND EARLY CORTICAL AUDITORY EVOKED RESPONSE IN MAN

The effect of increasing end-tidal enflurane concentration on the auditory evoked response was studied in six patients. After a standard induction, anesthesia was maintained with 70% nitrous oxide in oxygen and the end-tidal enflurane concentration was increased gradually from 0 to 1% over a period of 30 min. The averaged auditory evoked response was derived from the electroencephalogram and measurements were made of the latencies and amplitudes of waves I, III, V, Pa and Nb within the auditory evoked response. The latencies of all waves and the interpeak latencies I to V and III to V showed significant linear increases and the amplitudes of Pa and Nb showed significant linear decreases with increasing end-tidal enflurane concentration. These results could not be explained by changes in deep body temperature or end-tidal carbon dioxide concentration. The study demonstrated a dose-related direct effect of enflurane on the brainstem and early cortical components of the auditory evoked response.

Decreasing Enflurane Concentrations and d-Tubocurarine Neuromuscular Blockade

To study the effect of decreasing the concentration of enflurane on a combined enflurane-d-tubocurarine (dTC) neuromuscular blockade, six ASA class I or II patients were studied using a continuous infusion of dTC and a sequence of decreasing end-tidal concentrations of enflurane. A constant infusion of dTC and a 2.2 per cent end-tidal concentration of enflurane decreased twitch tension to 8 per cent of control. Maintaining this same infusion rate of dTC, but decreasing the end-tidal concentration of enflurane to 1.35 and 0.5 per cent, increased the twitch tension to 57 and 91 per cent of control, respectively. The authors conclude that the enflurane contribution to muscle relaxation dissipates in a dose-dependent manner as the end-tidal concentration of enflurane is reduced. This factor may provide additional safety for patients because the anesthetic produces a component of relaxation that is readily reversible with time without the use of acetylcholinesterase inhibitors.

Effects of Enflurane on Brainstem Auditory Evoked Responses in Humans

The effects of enflurane anesthesia on brainstem auditory evoked responses (BAERs) was determined in 10 patients with normal hearing undergoing various surgical procedures. Arterial blood pressure, body temperature, and arterial Pco2 were controlled during the 2- to 5-hour recording sessions. End-tidal enflurane concentrations were continuously recorded on a chemetron Medspect II mass spectrometer in three subjects. BAERs were obtained by, and recorded on a Nicolet CA 1000, from C2 with reference to A1 or !2, with a 2000 click-averaging for each measurement. Enflurane administered at clinical concentrations (0.5% to 3%) produced a consistent changes in BAER latencies. The waves significantly affected (p less than 0.01) were waves III, IV, and V and interpeak latency I-V. The magnitude of theses changes was related to the concentration of enflurane and was magnified by temporarily decreasing the Paco2. These findings confirm similar data obtained in animals which have shown the same effects at doses that can produce generalized seizure activity. BAER analysis shows that changes predominate at the pons and midbrain levels and affect the brain stem conduction time, which likely reflects the action of enflurane on the activity of the reticular activating system.

Decreasing enflurane concentrations and d-tubocurarine neuromuscular blockade.

To study the effect of decreasing the concentration of enflurane on a combined enflurane-d-tubocurarine (dTC) neuromuscular blockade, six ASA class I or II patients were studied using a continuous infusion of dTC and a sequence of decreasing end-tidal concentrations of enflurane. A constant infusion of dTC and a 2.2 per cent end-tidal concentration of enflurane decreased twitch tension to 8 per cent of control. Maintaining this same infusion rate of dTC, but decreasing the end-tidal concentration of enflurane to 1.35 and 0.5 per cent, increased the twitch tension to 57 and 91 per cent of control, respectively. The authors conclude that the enflurane contribution to muscle relaxation dissipates in a dose-dependent manner as the end-tidal concentration of enflurane is reduced. This factor may provide additional safety for patients because the anesthetic produces a component of relaxation that is readily reversible with time without the use of acetylcholinesterase inhibitors.

The pulmonary vasoconstrictor response to hypoxia during enflurane anesthesia.

Previous investigations have shown that diethyl ether, halothane and methoxyflurane inhibit the vasoconstrictor response to hypoxia in isolated rat lungs. A damping effect of diethyl ether and halothane has been observed in the human lung as well. In the intact dog lung, however, other workers have recently denied any effect of halothane and enflurane on this vasoconstrictor mechanism. These findings challenged us to investigate the effect of enflurane on the basoconstrictor response to hypoxia in isolated rat lungs. We found that enflurane administered via the airways reduced the response in proportion to the end-tidal concentration of enflurane, as determined by mass spectrometry.

Effects of Enflurane on Haemodynamics and Oxygen Consumption in the Dog with Special Reference‐ to the Liver and Preportal Tissues

The effects of enflurane anaesthesia on central circulation, total oxygen uptake, splanchnic circulation and splanchnic oxygen uptake were studied in 10 artifically ventilated dogs, basally anaesthetized with thiopental and nitrous oxide. Hepatic arterial, superior mesenteric arterial and portal venous blood flows were measured with electromagnetic flowmetry. Cardiac output was measured by thermodilution. Determinations of oxygen contents were made in arterial, pulmonary arterial, portal venous and hepatic venous blood. The end-tidal enflurane concentration was kept at about 1 MAC (= 2.2%). Arterial blood pressure diminished 54% of control value due to decreases of cardiac output to 65% and of total peripheral vascular resistance to 81% of control values. Hepatic arterial, superior mesenteric arterial and portal venous blood flows decreased to 65-70% of control levels and the corresponding vascular resistances all declined to about 80-85% of control values. Total oxygen uptake decreased, but less than cardiac output, leading to an increased arterio-venous oxygen content difference. Oxygen uptake of the preportal tissues was unchanged and hepatic oxygen uptake was not significantly altered, although there were decreases in hepatic oxygen uptake in some of the individual experiments. It is suggested that the cardiovascular depression following enflurane anaesthesia in the dog was due, to a great extent, to a primary myocardial depression. It is further concluded that the splanchnic blood flows were relatively well preserved, due to decreases in splanchnic vascular resistances, and that hepatic and preportal tissue oxygen consumptions were maintained by increased oxygen extraction.

Alteration by Enflurane of Electrophysiologic Correlates of Search in Short-term Memory

Effects of controlled subanesthetic concentrations of enflurane on short-term memory functions and associated scalp evoked potentials were studied in eight male volunteers. Short-term memory processes were assessed through a search task. A series of digits (one, three, five, seven, nine, or 11 digits in each series) was presented visually, followed by a test digit, which in half of the trials was part of the series, and in half of the trials was not. The subject responded by pressing one of two switches, signalling "yes" or "no" accordingly. Averaged evoked potentials elicited by the test digit were obtained from seven sites on the scalp. End-tidal enflurane concentrations between 0.12 and 0.25 per cent increased significantly by 30-40 msec the latency of the components of the evoked potentials reflecting sensory processing, but did not affect their amplitude significantly. This increase could not explain the 287-msec increase in reaction time. Amplitude of late components of the averaged potential reflecting information processing was markedly decreased, which the authors interpret as indicating increased trial-to-trial variation in latency of the late component. The authors conclude that enflurane delays and introduces variance into the short-term memory processes and subsequent decision processes that preced overt responses.