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PubMed1987

Low-dose enflurane as adjunct to high-dose fentanyl in patients undergoing coronary artery surgery: stable hemodynamics and maintained myocardial oxygen balance.

The effects of enflurane (end-tidal concentration 0.7%) on central and coronary hemodynamics and myocardial oxygenation were studied during steady state, high-dose fentanyl anesthesia in ten patients undergoing coronary artery bypass grafting operations. Compared with the response in ten patients receiving the same fentanyl anesthesia (100 micrograms/kg) without enflurane supplementation, enflurane caused a moderate reduction in mean arterial pressure, systemic vascular resistance, and left ventricular stroke work index. No patient showed signs of myocardial ischemia, and mean coronary sinus flow and calculated coronary resistance remained unchanged. Surgical stimulation induced no central or coronary hemodynamic responses in the enflurane-fentanyl group. No coronary hemodynamic changes occurred in the fentanyl group, but a marked increase in arterial pressure and systemic vascular resistance was seen. Myocardial oxygen extraction decreased in the enflurane supplemented group although it increased in the fentanyl group after surgical stimulation. Three fentanyl group patients and one enflurane-fentanyl group patient had a low myocardial lactate extraction as a sign of myocardial ischemia during surgery. We conclude that a 0.7% enflurane supplementation of 100 micrograms/kg fentanyl anesthesia does not endanger myocardial oxygenation and effectively prevents central and coronary hemodynamic responses to skin incision and sternotomy in patients undergoing coronary artery surgery.

Anesthesia, General↗
PubMed1985

Hormonal and hemodynamic responses to halothane and enflurane in spontaneously hypertensive rats.

Forty-two spontaneously hypertensive rats (SHR) and 42 normotensive Wistar-Kyoto rats (WKY) were anesthetized with either halothane or enflurane. Blood pressure, heart rate, cardiac output, distribution of blood flow, plasma renin activity, and plasma catecholamines were measured to determine in what manner the hypertensive animal responded to these two anesthetics. Major findings of the study were that plasma renin activity did not increase in the SHR despite a 25% reduction in MAP. The infusion of saralasin, an angiotensin II antagonist, resulted in a further decrease in blood pressure in SHR anesthetized with halothane but not with enflurane. Plasma catecholamine concentrations were elevated in the awake SHR and were decreased in SHR anesthetized with enflurane. Both halothane and enflurane anesthesia resulted in similar alterations in blood flow in the SHR. The normotensive WKY responded to halothane and enflurane in a different manner than the SHR. Plasma renin activity increased with the decrease in blood pressure with both agents. A further decrease in blood pressure occurred with saralasin infusion in WKY anesthetized with halothane or enflurane. Significant blood flow alterations occurred in the WKY anesthetized with both agents, but enflurane caused the greatest changes. The SHR may prove useful in examining the effects of anesthetic agents and other drugs so that we may have a better understanding of the perioperative management of the patients with essential hypertension.

Anesthesia, Inhalation↗
PubMed1984

[Blood pressure control with an inhalation anesthetic in acute intraoperative hypertension. Hemodynamic profile of halothane, enflurane and isoflurane in coronary surgery patients].

The haemodynamic effects of isoflurane, halothane and enflurane when used to control intraoperative hypertension were evaluated in 30 patients undergoing coronary artery bypass grafting. The patients were anaesthetized with flunitrazepam, fentanyl, pancuronium and N2O-O2. Control measurements were made after skin incision. When mean arterial pressure increased to 110 mmHg due to sternal spread or surgical manipulation of the aorta, halothane, enflurane or isoflurane were administered to return arterial pressure to control levels. Using a non-rebreathing system, inspired halothane concentrations of 1.0-1.5 vol.%, enflurane concentrations of 2.0-2.5 vol.% and isoflurane concentrations of 1.5-2.0 vol.% were necessary. Measurements were repeated during the hypertensive episodes and after treatment with halothane, enflurane or isoflurane while surgical stimulation continued. During the hypertensive episodes marked elevations in systemic vascular resistance were observed, four patients developed ischaemic ST-segment changes. Each of the three inhalational anaesthetics decreased mean arterial pressure to baseline values within 5 to 10 minutes. The fall in blood pressure caused by halothane was mainly due to a reduction in cardiac index, since the elevated systemic vascular resistance almost remained unaffected. Enflurane produced a similar fall in cardiac index, although left ventricular afterload was significantly reduced, suggesting that enflurane caused more impairment of cardiac performance than halothane. In contrast, the administration of isoflurane was associated with an increase of the cardiac index in the presence of marked systemic vasodilation and a slight decrease in left ventricular filling pressure. Halothane, enflurane and isoflurane reduced the rate-pressure product by a comparable degree and, when present, abnormalities in the ST-segments disappeared.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1983

Enflurane, halothane, and aminophylline--uptake and pharmacokinetics.

This study was designed to evaluate the effects of induction of enflurane or halothane anesthesia on the distribution and elimination of previously administered intravenous aminophylline, and to evaluate the effect of previously administered intravenous aminophylline on the uptake of enflurane or halothane. Fifty-four dogs were studied: 6 received no anesthetic, 24 received enflurane, and 24 halothane. The six animals receiving no anesthetic were given 10 mg/kg of aminophylline. In each of the two groups of 24 animals, six animals served as controls and received no aminophylline. Of the other 18 animals in each group, six received 10 mg/kg of aminophylline, six received 25 mg/kg of aminophylline, and six received 50 mg/kg of aminophylline intravenously before induction of enflurane or halothane anesthesia. The redistribution (alpha) phase of theophylline was similar when anesthesia was induced with either enflurane or halothane and slightly more rapid when no anesthetic was given following aminophylline administration. The elimination (beta) phase of theophylline in the presence of either anesthetic was not significantly different than when no anesthetic was administered. The uptake of enflurane or halothane was unaffected by prior administration of aminophylline. Differences in arrhythmogenicity between enflurane and halothane after aminophylline administration are not related to alterations in theophylline pharmacokinetics or anesthetic uptake.

Aminophylline↗
PubMed1982

Lack of toxicity of enflurane on male reproductive organs in mice.

Enflurane has been shown to increase slightly the percentage of abnormal spermatozoa in mice. To examine in more detail possible adverse effects of enflurane on male reproductive organs, 125 Swiss/ICR mice were exposed to 0.3% enflurane for up to 18 months; a control group of 125 mice was exposed concurrently to air. Exposures were for 4 hours/day, 5 days/week. After 12 months of exposure, groups of 25 enflurane-treated and control mice were killed, and chromosomal analysis of spermatogonial cells was performed. After 18 months exposure, remaining mice were killed and epididymal sperm were collected for morphologic examination. In addition, the reproductive organs of all mice dying or killed throughout the study were examined histologically. Approximately 1% of spermatogonial cells from both enflurane-treated and control mice had aberrant chromosomes. The average percentage of morphologically abnormal sperm was 9.4 +/- 1.7 for enflurane-treated mice and 6.5 +/- 1.3 for control mice; the difference was not statistically significant (p = 0.18). Finally, there was no difference between the treated and control mice in histologic appearance of reproductive organs. It was concluded that long-term exposure to enflurane has no adverse effects on male reproductive organs in mice.

Animals↗
PubMed1980

Metabolic and toxicologic studies with enflurane in Swiss/ICR mice.

Swiss/ICR mice were tested to determine whether the volatile ether anesthetic, enflurane, causes induction of anesthetic defluorination and organ toxicity. Mice were exposed in utero and postnatally to 0.01, 0.1 and 1.0 volumes percent enflurane vapor. Body weight was measured at frequent intervals throughout the experiment. Animals were sacrificed at 73 days of age and liver microsomal cytochrome P-450 content and the rate of defluorination of enflurane, isoflurane, methoxyflurane ans sevoflurane were determined. In addition, the liver, kidney and testis were weighed and examined histologically for drug induced damage. The maximum tolerated dose of enflurane delivered over a twelve week period was determined to be 0.5 volumes percent for four hours a day, five days a week. Even at this high dose there was no evidence in either sex of liver, kidney or testicular damage. Following enflurane exposure, neither the liver microsomal cytochrome P-450 content nor the rate of anesthetic defluorination was increased. The rate of in vitro inorganic fluoride production per unit time was greatest for methoxyflurane, and approximately equal for enflurane, isoflurane and sevoflurane. Since there was no evidence of enzyme induction or specific organ toxicity, it was concluded that enflurane is a comparatively nontoxic volatile anesthetic under conditions of this study.

Animals↗
PubMed1994

[A study on combined acupuncture and enflurane anesthesia for craniotomy].

The reinforcing effect of transcutaneous acupoint electric stimulation (TAES) with enflurane anesthesia during craniotomy was studied. 110 neurosurgical patients were randomly divided into three groups. Anesthesia was maintained with enflurane in group A (n = 40); in group B, enflurane anesthesia was supplemented by TAES with Han's acupoint nerve stimulator (HANS) at Hegu, Yuyao and Fengchi points on the operated side (n = 40); in group C, enflurane anesthesia was supplemented by TAES and scalp infiltration with 0.5% procaine (n = 30). The results showed that the minimum alveolar concentration (MAC) of enflurane in group B and C decreased 37.8-47.0% and 42.1-66.1% respectively than that in group A. The hemodynamics was more stable during operation, and the patients recovered faster after operation in group B and C. It was concluded that TAES with HANS significantly potentiated the anesthetic effect and decreased the side effects of enflurane during operation, and that the triple combination of TAES, enflurane and scalp infiltration with procaine proved to be a better anesthetic method for craniotomy.

Acupuncture Analgesia↗
PubMed1977

[Enflurane and fluorconcentrations in maternal and fetal blood during anaesthesia for for caesarean Section (authors transl)].

During anaesthesia for caesarean sections, the placental transfer and metabolism of Enflurane were investigated in 14 cases. In 3 cases, the administered concentration of 0.4 vol.% Enflurane showed too slight anaesthesia. In 11 cases, 0.6 vol.% Enflurane were delivered to the maternal respiratory mixture. A gaschromatographic method was used to measure the maternal and fetal blood concentrations of Enflurane. The calculated maternal mean value of Enflurane showed a concentration of 330 mumol/l which corresponds to 6.07 mg/100ml; the fetal mean value was 148 mumol/l or 2.72 mg/100 ml. This means that during operating time about 44.8% from the maternal Enflurane concentration has crossed to the fetus. The metabolic break down of Enflurane could be demonstrated by the measurement of inorganic fluorides in the maternal and fetal blood. The fluor concentration in the maternal blood increased during the operation and reached a mean value of 15.5 mumol/l at the time of birth; the mean value in the cord vein was at the same time 9.28 mumol/l which corresponds to 61% of the maternal concentration.

Anesthesia, Obstetrical↗
PubMed1975

Neuromuscular effects of enflurane, alone and combined with d-Tubocurarine, pancuronium, and succinylcholine, in man.

The neuromuscular effects of d-tubocurarine (dTc), pacuronium, and succinylcholien (SCh) were studied in 37 unpremedicated adult surgical patients anesthetized with 1.25 MAC enflurance in oxygen. The relaxant doses that produced 50 per cent depression of twitch height (ED50) were 1.57, 0.29, and 4.9 mg/m2 for dTc, pancuronium, and SCh, respectively. These doses are approximately 3.1, 1.7, and 1.0 times less than the amount of dTc, pancuronium, and SCh required to produce 50 per cent depression of twitch height during halothane anesthesia but are the same as ED50 values during isoflurane anesthesia. In eight additional unpremedicated patients anesthesia was maintained at 0.71 MAC enflurane in oxygen (five patients) or 1.67 MAC enflurane in oxygen (three patients). Twitch depression following dTc, 1.5 mg/m2, was related directly to alveolar enflurane concentration. Ability to sustain tetanus decreased progressively with increasing tetanic frequencies and decreased with increasing alveolar enflurane concentrations. The authors concluded that smaller doses of dTc and pancuronium are needed for adequate relaxation during enflurane anesthesia than during equi-MAC halothane anesthesia, and that higher alveolar enflurane concentrations reduce the dose of dTc necessary to produce a given amount of paralysis. Also, neuromuscular effects of enflurane in combination with dTc or pancuronium are not significantly different from those seen suring equi-MAC isoflurane anesthesia.

Anesthesia, Inhalation↗
PubMed1989

Concentration-related changes in the rate of CSF formation and resistance to reabsorption of CSF during enflurane and isoflurane anesthesia in dogs receiving nitrous oxide.

The rate of cerebrospinal fluid (CSF) formation (Vf) and resistance to reabsorption of CSF (Ra) were determined at four concentrations of enflurane (0.9, 1.8, 2.0, and 3.5% end-expired) or isoflurane (0.6, 1.1, 1.7, and 2.2% end-expired) in dogs receiving nitrous oxide (66%) in oxygen. At the two higher concentrations of enflurane, Vf was about 27% greater (38-40% greater when corrected for the effects of time) than at the two lower concentrations of enflurane. At the two lower concentrations of enflurane and at all doses of isoflurane, Vf did not differ between or within anesthetic groups (0.029-0.033 ml/min). The pattern of Ra data was more varied. Ra was elevated with the two lower concentrations of enflurane (by about 68%) and with isoflurane 1.1% (by about 33%), and reduced with the two higher concentrations of isoflurane (by about 14-17%). It is concluded that the effects of enflurane and isoflurane on CSF dynamics are concentration-related. All concentrations of enflurane studied favor CSF volume expansion, while high concentrations of isoflurane favor CSF volume contraction.

Journal Article↗
PubMed2001

Flumazenil improves cognitive and neuromotor emergence and attenuates shivering after halothane-, enflurane- and isoflurane-based anesthesia.

PURPOSE: To conduct a randomized, placebo-controlled, double-blinded, clinical experiment testing the hypothesis that flumazenil, a benzodiazepine antagonist, may affect recovery from halothane-, enflurane- and isoflurane-based anesthesia. METHOD: Patients who underwent surgery under N(2)O/O(2) plus halothane (n=100), enflurane (n=100) or isoflurane (n=70) anesthesia were administered flumazenil 1 mg or placebo upon emergence from anesthesia, and their postanesthesia vital signs, vigilance, neurological recovery, shivering, amnesia reversal, and general subjective feeling were assessed. RESULTS: A ten-point vigilance score showed better recovery of flumazenil-treated patients compared to those who received placebo (60-min after halothane anesthesia: 9.9 +/- 0.1 vs 9.5 +/- 0.2, P <0.01; after enflurane: 10 +/- 0 vs 9.4 +/- 0.2, P <0.01; after isoflurane: 10.0 +/- 0 vs 9.3 +/- 0.1, P <0.01). Halothane- and enflurane-flumazenil-treated patients (but not isoflurane) reached a better neurological score (2.97 +/- 0.05 or 3 +/- 0) compared to placebo (2.8 +/- 0.4 or 2.6 +/- 0.4, P <0.01), respectively. Reversal of amnesia was superior in the flumazenil group at 60 min and at 24 hr postsurgery, and more flumazenil patients rated recovery as "pleasant". Flumazenil patients shivered less than placebo patients despite their lower core temperature (at 30 min: halothane: 11% vs 28%, P <0.05; enflurane: 11% vs 30%, P <0.05; isoflurane: 17% for both groups). CONCLUSION: Flumazenil improves recovery of high cortical and neuromotor functions following halothane, enflurane and isoflurane anesthesia, reduces shivering and improves the overall quality of emergence, including patients' subjective feeling.

Adult↗
PubMed2002

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

PURPOSE: To investigate the effects of caudal analgesia on the minimal alveolar concentration of enflurane for laryngeal mask airway (LMA) smooth extubation (MACex). METHODS: 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. RESULTS: 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%). CONCLUSION: 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.

Anesthesia, Caudal↗
PubMed1995

Quantifying the effect of enflurane on atracurium infusion requirements.

The present study was designed to evaluate the interaction between atracurium and enflurane in 40 adult surgical patients using closed-loop feedback control of infusions of atracurium. Anaesthesia was induced with thiopentone and fentanyl and intubation was facilitated with atracurium 0.5 mg.kg-1 lean body mass. During the first 90 min, anaesthesia was maintained with nitrous oxide in oxygen (2:1) and fentanyl. For the following 90 min the patients were randomly assigned to receive enflurane at different end-tidal concentrations: Group I, control, fentanyl-nitrous oxide anaesthesia; Group II, enflurane 0.3%-nitrous oxide; Group III, enflurane 0.6%-nitrous oxide; Group IV, enflurane 0.9%-nitrous oxide. The possible interaction of atracurium with enflurane was quantified by determining the asymptotic steady-state rate of infusion (ISS) of atracurium necessary to produce a constant 90% neuromuscular block. This was accomplished by applying nonlinear curve fitting to data on the cumulative dose requirements. Every patient served as his/her own control and the changes in the infusion rates were determined individually. Patient characteristics and controller performance, i.e., the ability of the controller to maintain the neuromuscular blockade constant at the setpoint, did not differ among groups. In Group II ISS decreased from 0.33 +/- 0.12 to 0.26 +/- 0.08 mg.kg-1.hr-1 (P < 0.01), in Group III from 0.32 +/- to 0.12 to 0.24 +/- 0.08 mg.kg-1.hr-1 (P < 0.001) and in Group IV from 0.29 +/- 0.09 to 0.21 +/- 0.09 mg.kg-1.hr-1 (P < 0.001). In the control group atracurium requirements remained unchanged throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

A comparative analysis of enflurane anesthesia on primate motor and somatosensory evoked potentials.

The effect of increasing enflurane concentration on magnetic-induced myogenic cranial (Cr) and peripheral (Pr) motor evoked potentials (MEPs), and electrically induced median (MN) and posterior tibial (PTN) somatosensory evoked potentials (SEPs) was studied in 10 monkeys. MEP, recorded from abductor pollicis brevis and abductor hallucis muscles, and SEP (short- and long-latency scalp recorded potentials) variables were examined at 0.25, 0.5, 0.75, 1.0 MAC enflurane concentrations. Cr-MEPs progressively attenuated (P less than 0.01) with 0.25 MAC and were abolished (greater than or equal to 0.75 MAC) by graded enflurane concentration. Stimulation threshold for Cr-MEP was progressively elevated (P less than 0.01), and eventually reliable responses were lost (greater than or equal to 0.75 MAC). Marked scalp zone reduction to obtain Cr-MEP responses was noted with increasing enflurane concentration. Pr-MEPs and most SEP peaks maintained good replicability but showed significant amplitude reduction (P less than 0.01). MEP and SEP latency values were not significantly delayed as long as the wave form remained identifiable. We conclude that enflurane has a differential influence on Cr-MEPs and SEPs. Administration of enflurane should be discouraged while monitoring myogenic Cr-MEPs since even a subanesthetic concentration is profoundly detrimental.

Analysis of Variance↗
PubMedDate not supplied

Determination of volatile anesthetics isoflurane and enflurane in mouse brain tissues using gas chromatography-mass spectrometry.

INTRODUCTION: A method for determination of the volatile anesthetics, isoflurane, and enflurane in mouse brain tissues using headspace gas chromatography-mass spectrometry (GC-MS) is described. METHODS: Halothane was used as internal standard (I.S.). Brain samples were completely homogenized in ice-cold water and isoflurane, enflurane, and I.S. were extracted with headspace. One milliliter of headspace gas was injected onto the GC-MS and separation was achieved by using porous layer open tubular (PLOT) capillary column with a solid stationary phase (GSC). As a result, isoflurane, enflurane, and halothane were cleanly separated. RESULTS: The method demonstrated satisfactory recovery (72% and 76% for isoflurane and enflurane, respectively) and linear calibration ranges of 0.015-2.20 and 0.0152-3.94 microg/sample for isoflurane and enflurane, respectively. Reproducibility calculated as CV% was 3.3-3.9% for all intraday and interday determinations. The procedure was applied for quantitation of isoflurane and enflurane in about 300 mouse brain samples for genetic behavioral study. DISCUSSION: The method was achieved and shown to be effective.

Anesthetics, Inhalation↗
PubMed1985

[Enflurane and extracorporeal circulation. Peripheral vascular effects and consequences of hypothermia on its biotransformation].

The effects of enflurane on systemic vascular resistance and venous capacitance, and its biotransformation during hypothermia, were studied in patients undergoing cardiovascular surgery with enflurane anaesthesia. When administered during cardiopulmonary bypass (CPB), cardiac regulatory mechanisms being therefore excluded, enflurane induced an arteriolar vasodilation related to the concentration inhaled. An inspired concentration of 2.5% in hypothermia (28 degrees C) produced a drop in systemic vascular resistance of 30% from control level. In the same conditions, venous capacitance was not altered. The rise in the blood gas solubility coefficient during hypothermia was only partly balanced by haemodilution. Therefore, inspired enflurane concentration should be higher during hypothermic CPB than during normothermic anaesthesia to obtain the same effects. For the same amount of enflurane inhaled, the fraction of enflurane metabolized was higher in hypothermia than in normothermia, but the inorganic fluoride plasma concentration at its highest never reached the level of 50 mumol X 1(-1) regarded as the nephrotoxic threshold.

Adult↗
PubMed1997

Influence of 0.2 minimum alveolar concentration of enflurane on the ventilatory response to sustained hypoxia in humans.

To determine the influence of 0.2 minimum alveolar concentration (MAC) of enflurane on the time course of ventilation during sustained hypoxia, we studied 10 healthy adult volunteers with and without enflurane. The following design was used: end-tidal Po2 was maintained at 13.3 kPa for 8 min, at 6.7 kPa for 20 min and at 13.3 kPa for 8 min. End-tidal Pco2 was held constant throughout at 0.67 kPa above the subject's natural value. Control experiments were conducted with no hypoxia imposed. During the experiment subjects breathed via a mouthpiece from an automated gas mixing system which controlled end-tidal values. Enflurane reduced baseline (euoxic) ventilation from 20.9 (SEM 2.0) litre min-1 to 10.1 (1.0) litre min-1 (ANOVA, P < 0.001). Enflurane reduced the acute ventilatory response to hypoxia (AHVR) from 20.1 (3.3) litre min-1 to 5.0 (1.3) litre min-1 (ANOVA, P < 0.01), and the ventilatory off-response at cessation of hypoxia from 11.7 (2.4) litre min-1 to 1.8 (0.5) litre min-1 (ANOVA, P < 0.02). There was no significant difference in hypoxic ventilatory decline (HVD) without and with enflurane (8.9 (2.4) litre min-1 vs 5.5 (1.1) litre min-1; ANOVA, ns). These results confirm that 0.2 MAC of enflurane suppressed the acute ventilatory response to hypoxia, but had no significant effect on the subsequent ventilatory decline during sustained hypoxia.

Adult↗
PubMed1993

Enflurane inhibits NMDA, AMPA, and kainate-induced currents in Xenopus oocytes expressing mouse and human brain mRNA.

Effects of enflurane, an inhalational anesthetic, on NMDA, AMPA, and kainate-gated currents were examined in Xenopus laevis oocytes expressing mouse or human brain mRNA. In oocytes expressing mouse mRNA, enflurane at an anesthetic concentration (1.8 mM) inhibited the NMDA-, AMPA-, and kainate-induced currents by 29-40%, 30-33%, and 20-27%, respectively, suggesting that all three glutamate ionotropic receptors are susceptible to suppression by inhalational anesthetics. Furthermore, inhibition by enflurane was independent of the concentrations of the agonists (NMDA, AMPA, and kainate) or the NMDA-coagonist (glycine). This suggests that enflurane inhibition does not result from a competitive interaction at glutamate or glycine binding sites. Enflurane also suppressed the oscillation and apparent desensitization of NMDA currents, suggesting an inhibition of Ca2+ influx through the NMDA channel. In oocytes expressing human brain mRNA, only kainate produced observable currents. Kainate currents of human channels were smaller in size than those of the mouse; however, the kainate concentration-response curve and percent inhibition (27-29%) by enflurane were similar for mice and humans. The results suggest that human and mouse kainate receptors have similar pharmacological characteristics.

Aged↗