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At least 109 records · Page 6Linked to original sources
PubMed2000

Enflurane directly depresses glutamate AMPA and NMDA currents in mouse spinal cord motor neurons independent of actions on GABAA or glycine receptors.

BACKGROUND: The spinal cord is an important anatomic site at which volatile agents act to prevent movement in response to a noxious stimulus. This study was designed to test the hypothesis that enflurane acts directly on motor neurons to inhibit excitatory synaptic transmission at glutamate receptors. METHODS: Whole-cell recordings were made in visually identified motor neurons in spinal cord slices from 1- to 4-day-old mice. Excitatory postsynaptic currents (EPSCs) or potentials (EPSPs) were evoked by electrical stimulation of the dorsal root entry area or dorsal horn. The EPSCs were isolated pharmacologically into glutamate N-methyl-d-aspartate (NMDA) receptor- and non-NMDA receptor-mediated components by using selective antagonists. Currents also were evoked by brief pulse pressure ejection of glutamate under various conditions of pharmacologic blockade. Enflurane was made up as a saturated stock solution and diluted in the superfusate; concentrations were measured using gas chromatography. RESULTS: Excitatory postsynaptic currents and EPSPs recorded from motor neurons by stimulation in the dorsal horn were mediated by glutamate receptors of both non-NMDA and NMDA subtypes. Enflurane at a general anesthetic concentration (one minimum alveolar anesthetic concentration) reversibly depressed EPSCs and EPSPs. Enflurane also depressed glutamate-evoked currents in the presence of tetrodotoxin (300 nm), showing that its actions are postsynaptic. Block of inhibitory gamma-aminobutyric acid A and glycine receptors by bicuculline (20 micrometer) or strychnine (2 micrometer) or both did not significantly reduce the effects of enflurane on glutamate-evoked currents. Enflurane also depressed glutamate-evoked currents if the inhibitory receptors were blocked and if either D,L-2-amino-5-phosphonopentanoic acid (50 micrometer) or 6-cyano-7-nitroquinoxaline-2,3-dione disodium (10 micrometer) was applied to block NMDA or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-kainate receptors respectively. CONCLUSIONS: Enflurane exerts direct depressant effects on both alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and NMDA glutamate currents in motor neurons. Enhancement of gamma-aminobutyric acid A and glycine inhibition is not needed for this effect. Direct depression of glutamatergic excitatory transmission by a postsynaptic action on motor neurons thus may contribute to general anesthesia as defined by immobility in response to a noxious stimulus.

2-Amino-5-phosphonovalerate↗
PubMed2006

Dual actions of enflurane on postsynaptic currents abolished by the gamma-aminobutyric acid type A receptor beta3(N265M) point mutation.

BACKGROUND: At concentrations close to 1 minimum alveolar concentration (MAC)-immobility, volatile anesthetics display blocking and prolonging effects on gamma-aminobutyric acid type A receptor-mediated postsynaptic currents. It has been proposed that distinct molecular mechanisms underlie these dual actions. The authors investigated whether the blocking or the prolonging effect of enflurane is altered by a point mutation (N265M) in the beta3 subunit of the gamma-aminobutyric acid type A receptor. Furthermore, the role of the beta3 subunit in producing the depressant actions of enflurane on neocortical neurons was elucidated. METHODS: Spontaneous inhibitory postsynaptic currents were sampled from neocortical neurons in cultured slices derived from wild-type and beta3(N265M) mutant mice. The effects of 0.3 and 0.6 mm enflurane on decay kinetics, peak amplitude, and charge transfer were quantified. Furthermore, the impact of enflurane-induced changes in spontaneous action potential firing was evaluated by extracellular recordings in slices from wild-type and mutant mice. RESULTS: In slices derived from wild-type mice, enflurane prolonged inhibitory postsynaptic current decays and decreased peak amplitudes. Both effects were almost absent in slices from beta3(N265M) mutant mice. At clinically relevant concentrations between MAC-awake and MAC-immobility, the anesthetic was less effective in depressing spontaneous action potential firing in slices from beta3(N265M) mutant mice compared with wild-type mice. CONCLUSION: At concentrations between MAC-awake and MAC-immobility, beta3-containing gamma-aminobutyric acid type A receptors contribute to the depressant actions of enflurane in the neocortex. The beta3(N265M) mutation affects both the prolonging and blocking effects of enflurane on gamma-aminobutyric acid type A receptor-mediated inhibitory postsynaptic currents in neocortical neurons.

Action Potentials↗
PubMed1981

Metabolic ability and enflurane defluorination in surgical patients.

Antipyrine clearance and half-life, which are measures of the hepatic metabolic ability, were determined prior to anaesthesia in 14 surgical patients. The antipyrine results correlated neither with the highest serum fluoride concentrations nor with the fluoride excretion in urine following administration of enflurane. Enzyme induction may therefore have little influence on enflurane metabolism in man. Inorganic fluoride concentrations in serum and in excreted urine were determined following the exposure of a total of 21 surgical patients to measured doses of enflurane. In the group of 14 patients tested for metabolic ability, a mean dose of 0.4 end-tidal vol. % X h enflurane resulted in a mean peak serum fluoride concentration of 6.8 mumol/l (maximum 13.6 mumol/l) 2 h after enflurane exposure. In the material as a whole, the enflurane dose was positively correlated with both post-anaesthetic highest serum fluoride concentrations and the 24-h post-anaesthetic urine pH (P less than 0.01) as well as urinary volume and fluoride excretion in urine during that time. At a urinary pH below 5.0, the fluoride excretion was very low, while the highest excretions were associated with a urinary pH of about 7.0. Raising the patient's per- and post-anaesthetic urine pH and maintaining a good urinary output (which also tends to increase urine pH) may be enough to prevent accumulation of inorganic fluoride in the body following enflurane anaesthesia.

Adolescent↗
PubMed1995

Quantifying the interaction of vecuronium with enflurane using closed-loop feedback control of vecuronium infusion.

The influence of different levels of enflurane anaesthesia on infusion requirements of vecuronium was studied in 40 adult surgical patients. Ninety percent neuromuscular block was maintained by computer controlled infusion of vecuronium. During the first 90 min study period all patients received fentanyl-nitrous oxide-oxygen (2:1) anaesthesia. 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. Every patient served as his/her own control and the changes of vecuronium infusion requirements were determined individually. When the administration of enflurane was started, vecuronium infusion requirements decreased progressively until 90 min. In group II the infusion rate lowered from 80 +/- 28 to 56 +/- 20 micrograms.kg-1.h-1, in group III from 61 +/- 29 to 34 +/- 17 micrograms.kg-1.h-1 and in group IV from 65 +/- 20 to 30 +/- 14 micrograms.kg-1,h-1. In the control group the infusion rate decreased during the three hour study period from 69 +/- 17 (first 90 min period) to 59 +/- 16 micrograms.kg-1.h-1 (second 90 min period). Enflurane reduces the dose requirements of vecuronium administered by continuous infusion in a dose- and time-dependent manner.

Adolescent↗
PubMed1994

The effects of propofol and enflurane on single calcium channel currents of guinea-pig isolated ventricular myocytes.

1. The effects of the anaesthetics, propofol (100 microM) and enflurane (3%, 1.46 mM), on single L type calcium channel currents were investigated in single myocytes isolated from guinea-pig ventricles. Channel activity was recorded from membrane patches by use of the 'cell-attached' patch-clamp technique (pipette solution containing 110 mM BaCl2, 5 microM Bay K 8644, 5 microM HEPES, pH 7.4; temperature 36 degrees C). 2. Channel conductance was calculated from the slope of the relationship between single channel current and membrane potential during step depolarizations to activate the channel over a range of approximately -20 to +20 mV. Neither propofol (6 cells) nor enflurane (7 cells) caused any significant reduction in channel conductance. 3. Both propofol (7 cells) and enflurane (9 cells) decreased the probability of the channel being open during depolarizations to +10 mV (measured from histograms of the fraction of time spent by the channel at different current levels, taking areas under the Gaussian curves fitted to the open and closed components of the distributions to represent the proportion of time spent in the two states). 4. A fraction of the current traces showed no detectable channel openings in response to step depolarizations to +10 mV. Both propofol and enflurane significantly increased the fraction of silent traces. 5. Transitions across a threshold halfway between the open and closed levels were used to define periods spent in the open and closed states. Both propofol (7 cells) and enflurane (9 cells) reduced the mean open times and increased the mean closed times of the calcium channel. 6. Histograms were plotted showing the distributions of times spent by the channels in the open and closed states. Two exponentials were fitted to the open and closed time distributions. Both propofol (7 cells) and enflurane (9 cells) shortened both time constants fitted to the open times and lengthened both time constants fitted to the closed times.7. It is concluded that both propofol and enflurane appear to alter the kinetics of opening and closing of calcium channels to favour shut channels without altering channel conductance. This effect would be expected to result in a reduction of the macroscopic calcium current and thus contribute to the negative inotropic action of these anaesthetics.

Animals↗
PubMedDate not supplied

Effects of thiopental, ketamine, diazepam, xylazine, and nitrous oxide on EEG spike activity and convulsive behavior during enflurane anesthesia in atropinized cats. Effect of increasing inhalant concentrations.

The effects of thiopental, ketamine, diazepam, xylazine, and nitrous oxide, and the combinations of thiopental-nitrous oxide and ketamine-nitrous oxide, on both enflurane-induced electroencephalographic (EEG) spike activity and convulsive behavior were measured quantitatively in atropinized cats receiving enflurane with controlled ventilation. Pretreatments with thiopental, ketamine, and diazepam reduced both EEG spike frequency and amplitude at 2.5% to 4.5% inspired enflurane but did not abolish spike activity. Nitrous oxide (66% of inspired gas) did not significantly alter spike frequency or amplitude during 2.5% to 4.5% inspired enflurane, but the combination of thiopental-nitrous oxide or ketamine-nitrous oxide reduced EEG spike activity during 2.5% inspired enflurane. Enflurane-induced convulsive score was markedly suppressed by thiopental and ketamine and was significantly reduced by diazepam, xylazine and nitrous oxide. The combinations of thiopental-nitrous oxide and ketamine-nitrous oxide greatly reduced behavioral-convulsive responses induced by 2.5% to 4.5% inspired enflurane.

Anesthesia, Inhalation↗
PubMedDate not supplied

Effects of thiopental, ketamine, diazepam, xylazine, and nitrous oxide on EEG spike activity and convulsive behavior during enflurane anesthesia in spontaneously breathing atropinized cats. Effect at surgical depth.

The effects of thiopental, ketamine, diazepam, xylazine and nitrous oxide, and combinations of thiopental-nitrous oxide and ketamine-nitrous oxide on electroencephalographic (EEG) spike activity and convulsive behaviors in atropinized cats at surgical depth of enflurane anesthesia were assessed quantitatively for 60 minutes during spontaneous ventilation. Mean inspired enflurane concentrations (MIEC) were reduced 16% to 29% by pretreatment with thiopental, ketamine, diazepam, and xylazine, and were reduced 19% by 66% nitrous oxide. The MIEC of cats anesthetized with thiopental-nitrous oxide-enflurane and ketamine-nitrous oxide-enflurane were 35% to 38% lower than that with nitrous oxide-enflurane. Pretreatment with thiopental, ketamine, diazepam, and xylazine did not reduce the EEG spike frequency during anesthesia but did markedly reduce the spike amplitude. The addition of 66% nitrous oxide did not alter the spike frequency during anesthesia but tended to reduce the spike amplitude. Combinations of thiopental-nitrous oxide and ketamine-nitrous oxide almost abolished the spike activity. The addition of 66% nitrous oxide prevented convulsive responses elicited by photic and auditory stimulation during enflurane anesthesia. Treatment with thiopental, ketamine, diazepam and xylazine, and combinations of thiopental-nitrous oxide and ketamine-nitrous oxide, completely prevented convulsive responses during enflurane anesthesia.

Anesthesia, Inhalation↗
PubMed1978

Enflurane nephrotoxicity and pre-existing renal dysfunction.

This study provides the first morphological evidence of significant structural damage following high doses of enflurane alone and confirms previous findings of transient renal functional abnormalities following high dosage enflurane. The study also indicates that enflurane may have a greater potential for renal toxicity in the presence of renal impairment. Treatment of Fischer 344 rats with a nephrotoxic dose of gentamicin prior to six hours of enflurane (GE) anaesthesia at 1 MAC resulted in increased serum concentration of the enflurance metabolite inorganic fluoride (GE, 43.9 +/- 1.5; E, 34.5 +/- 1.8 mu mol/L), increased urine flow rate and a greater degree of structural damage in renal proximal convoluted tubule cells than was observed with either gentamicin (G) or enflurane (E) alone. Treatment with gentamicin prior to enflurane also resulted in reduced urinary osmolality compared to enflurane or gentamicin alone (GE, 742 +/- 57; E, 1709 +/- 66; G, 985 +/- 32 m0sm/kg).

Anesthesia, Inhalation↗
PubMed1992

Halothane- and enflurane-induced inhibition of phasic responses to carbachol in isolated guinea pig trachea.

Volatile anesthetics produce bronchodilatation by a combination of effects on the autonomic nervous system as well as direct effects on the airway smooth muscle. We sought to further explain the direct effects on airway smooth muscle by studying the effect of volatile anesthetics on the phasic and tonic components of the contractile response. The effects of 1.2%, 2.3%, and 4.3% halothane and 1.6%, 3.2%, 4.9%, and 8.7% enflurane on the phasic and tonic components of the contractile response to 10 microM carbachol and 40 mM KCl in isolated guinea pig trachea were determined using steady-state and kinetic analyses. No direct effect of either anesthetic on resting tension was observed. The peak tensions of the phasic responses to 10 microM carbachol were significantly inhibited by all concentrations of halothane and enflurane. The inhibition by enflurane was concentration-dependent and eliminated the phasic response at 8.7%. The peak tensions of the tonic responses to 10 microM carbachol were unaffected. The peak tensions of the responses to 40 mM KCl were unaffected by halothane but were significantly inhibited by 4.9% enflurane. The decay rate of the phasic response was unaffected by the anesthetics. The onset rate of the tonic response was significantly inhibited only by 8.7% enflurane, whereas halothane was without effect. The EC50 concentration for carbachol, as determined by cumulative concentration response curves, was increased by both 8.7% enflurane and 4.3% halothane. The results support the hypothesis that halothane and enflurane inhibit that portion of the contractile response to carbachol dependent on the release of intracellular Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Enflurane decreases glutamate neurotransmission to spinal cord motor neurons by both pre- and postsynaptic actions.

UNLABELLED: We have previously reported volatile anesthetic actions on glycinergic inhibitory transmission to spinal motor neurons. The present study is a comparable set of experiments on glutamatergic excitatory transmission. We tested the hypothesis that the balance between excitation and inhibition is shifted toward inhibition by larger depressant actions on excitation. Patch-clamp techniques were used to study spontaneous and evoked glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid currents in rat spinal cord slices. Enflurane (0.6 mM, 1 minimum alveolar anesthetic concentration) significantly decreased spontaneous miniature current frequencies either when sodium channels were blocked (miniature excitatory postsynaptic currents, mEPSCs), or when sodium channels were not blocked (spontaneous excitatory postsynaptic currents, sEPSCs). Enflurane did not affect mEPSC or sEPSC amplitude or kinetics. The effects on mEPSCs and sEPSCs did not differ. Enflurane significantly decreased both amplitude and area of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-evoked currents with no change in kinetics (P < 0.05 and 0.01, respectively). In contrast, enflurane increased miniature glycinergic current frequency when sodium channels were blocked, and prolonged glycinergic current duration. Enflurane actions on glutamatergic excitatory transmission are purely depressant both pre- and postsynaptically, whereas glycinergic inhibition is enhanced presynaptically under some conditions, and always prolonged postsynaptically. Thus, enflurane shifts the balance between synaptic excitation and inhibition in the direction of inhibition. IMPLICATIONS: Explanations proposed for anesthetic-induced central nervous system depression include enhancement of synaptic inhibition and depression of excitation. The results reported herein suggest that, in the case of enflurane, the mechanism is a shift in the balance toward inhibition. Excitation is uniformly depressed by multiple mechanisms, whereas some anesthetic actions tend to enhance inhibition.

Anesthetics, Inhalation↗
PubMed1994

Comparison of plasma inorganic fluoride concentration with sevoflurane-N2O and enflurane-N2O anesthesia.

Plasma inorganic fluoride concentrations were measured in adult patients without hepatic or renal disease following sevoflurane-N2O anesthesia (n = 7) or enflurane-N2O anesthesia (n = 6). The anesthetic dosage of sevoflurane and enflurane was 6.48 +/- 2.15 %-hours and 6.57 +/- 2.50 %-hours, respectively. The mean peak plasma inorganic fluoride concentration in the sevoflurane group was 19.5 +/- 13.4 mumol/L 1 hour after anesthesia, which decreased to preanesthetic levels 24 hours after anesthesia. In the enflurane group the values were 13.2 +/- 5.8 mumol/L at the end of anesthesia and decreased, but remained, still twice as high as the preanesthetic level 24 hours after anesthesia. The relationship of plasma inorganic fluoride concentration and anesthetic dosage was more pronounced in the sevoflurane group (r = 0.68, slope = 4.2) than in the enflurane group (r = 0.39, slope = 1.2). In conclusion, sevoflurane-N2O anesthesia results in similar subnephrotoxic levels of plasma inorganic fluoride as enflurane-N2O anesthesia, and although the fluoride concentration had a better correlation to anesthetic dosage in the sevoflurane group than in the enflurane group, its excretion was faster in the sevoflurane group than in the enflurane group.

Adolescent↗
PubMedDate not supplied

Effect of enflurane on selected neuropeptides and marker enzymes in rabbit brain.

The aim of this study was to evaluate the effect of 5-, 15-, and 60-min enflurane anesthesia on the levels of Met-enkephalin, Leu-enkephalin and neuropeptide Y in discrete areas of the rabbit brain. We also evaluated the effect of enflurane anesthesia on energetic, transport and catabolic processes by measuring the activities of succinate dehydrogenase, magnesium-dependent adenosine triphosphatase and acid phosphatase in the rabbit striatum and hypothalamus. Induction of anesthesia (5 min) decreased Met-enkephalin levels in the hypothalamus and striatum, and increased them in the hippocampus and mesencephalon. Induction of anesthesia increased Leu-enkephalin levels in all brain areas studied, except for the striatum, and increased neuropeptide Y content in the hippocampus. 15- and 60-min enflurane anesthesia increased Met-enkephalin content in the hypothalamus and hippocampus. After 15- and 60-min anesthesia, and after cessation of anesthesia, Leu-enkephalin levels were increased in the hypothalamus and mesencephalon, and were decreased in the striatum and hippocampus. In the striatum, neuropeptide Y content was significantly decreased during anesthesia and after cessation of anesthesia. Histochemical analysis revealed that enflurane enhanced ATP production, catabolic processes, and the rates of exchange and transport of energetic substrates in the striatum and hypothalamus. In conclusion, enflurane affects the levels of Met, Leu-enkephalins and NPY in a manner depending on the duration of anesthesia and the brain structure. Compared with isoflurane , which was studied in our previous study enflurane produces stronger alterations in the activities of enzymatic marker in the rabbit brain. This suggests that enflurane may be less safe than isoflurane.

Acid Phosphatase↗
PubMed1990

Differences in effects of isoflurane and enflurane on splanchnic oxygenation and hepatic metabolism in the pig.

The effects of end-tidal concentrations of 1.45% isoflurane and 2.12% enflurane on splanchnic blood flow (electromagnetic flow probes), oxygen (O2) extraction and surface PO2 (Clark-type electrode), and hepatic metabolism (organic acids) were compared in an animal model relevant to humans. Eighteen laparotomized, ventilated pigs, anesthetized and paralyzed with ketamine/flunitrazepam and pancuronium, were studied. Enflurane caused significantly (P less than 0.05) greater decreases in mean arterial pressure, cardiac output, and superior mesenteric arterial, portal, and total hepatic blood flows. In addition, hepatic arterial blood flow decreased during enflurane administration but increased markedly (40%) during isoflurane administration. However, mean surface PO2 of liver and small intestine decreased to similar degrees (20%) during isoflurane and enflurane. Summary histograms of surface PO2 values were leftward shifted but did not show O2 values in the hypoxic range (0-5 mm Hg). Except for a decrease in hepatic lactate uptake during enflurane, there were no changes in either hepatic uptake or release of organic acids during anesthesia with either agent. These data show that splanchnic O2 supply is better maintained during isoflurane than during enflurane. Although this was not reflected in differences in tissue oxygenation and metabolism, decreased portal and hepatic venous O2 contents during enflurane indicate that an increase in preportal and hepatic oxygen extraction was necessary to preserve tissue oxygenation.

Animals↗
PubMed1989

Hypotensive anesthesia with isoflurane and enflurane during total hip replacement: a comparative study of catecholamine and renin angiotensin responses.

Catecholamine and renin-angiotensin responses to enflurane- or isoflurane-hypotensive anesthesia were compared in a randomized study. Two groups of 10 patients undergoing total hip arthroplasty were premedicated with morphine hydrochloride (0.1 mg/kg). Anesthesia was induced with thiopental and the trachea intubated after pancuronium. Equal concentrations of each volatile agent (1.3 MAC) were administered until mean arterial blood pressure decreased to 50-60 mm Hg. Hemodynamic data and blood samples for measurements of plasma renin activity (PRA) and plasma epinephrine (E) and norepinephrine (NE) concentrations were collected 1) after induction and intubation but before the start of isoflurane or enflurane; 2) 15 min (T15) after the start of isoflurane or enflurane administration; and 3) 45 min (T45) after the start of isoflurane or enflurane administration. The desired level of hypotension was achieved at T15 with isoflurane and at T45 with both anesthetics. When hypotension was achieved, cardiac index and stroke index were significantly lower in the enflurane group while systemic vascular resistance index was lower in the isoflurane group. Increases in E and NE levels above baseline levels were significantly greater in the isoflurane group than in the enflurane group. Use of isoflurane to induce hypotension is associated with more rapid induction of hypotension, less depression of cardiac output, and better preservation of homeostatic responses than is use of enflurane.

Enflurane↗
PubMed1987

[Effect of isoflurane and enflurane on somatosensory evoked potentials following stimulation of the median nerve].

The effects of enflurane and isoflurane on somatosensory evoked potentials (SEP) after median nerve stimulation were studied in 25 healthy adult patients. Cervical and cortical SEP were recorded simultaneously. pCO2 and tympanic membrane temperature were kept constant. Following induction of anaesthesia with thiopentone, fentanyl and succinylcholine SEP were recorded during normoventilation with 100% oxygen and after inhalation of 66.6% nitrous oxide. Isoflurane at inspired concentrations of 0.8, 1.65, 2.5, 3.3% was given to 10 patients at 15 minutes intervals and was reduced after nitrous oxide had been replaced by oxygen. 15 patients received equipotent doses of enflurane (1.1, 2.2, 3.25, 4.3%.) SEP were recorded at the end of each interval. Isoflurane and enflurane caused dose dependent increases in latency of the cortical SEP. This effect was more pronounced with enflurane. Isoflurane reduced amplitude of the primary cortical response more than enflurane, when ventilation was performed with 66.6% nitrous oxide in oxygen. High doses of enflurane in oxygen augmented cortical SEP amplitudes associated with a marked increase in latency. Isoflurance and enflurance anaesthesia slightly altered cervical SEP. Middle latency components of the cortical SEP were progressively diminished with increasing isoflurane or enflurane concentrations. The effect of both agents in terms of delayed latencies and reduced amplitudes should be considered when recordings are performed intraoperatively.

Adolescent↗
PubMed1986

Comparison of sufentanil and enflurane-nitrous oxide anesthesia for myocardial revascularization.

This study compared the stress response in patients with coronary artery disease undergoing myocardial revascularization anesthetized with either sufentanil and oxygen or enflurane-nitrous oxide and oxygen. Throughout induction and maintenance of anesthesia, and while the patients were in the intensive care unit, hemodynamics plus plasma catecholamine, sufentanil, and enflurane concentrations were recorded and compared. Three groups were studied: sufentanil, 15 micrograms/kg at induction; sufentanil, 15 micrograms/kg at induction plus 10 micrograms/kg on initiation of cardiopulmonary bypass (CPB); and enflurane anesthesia. Hemodynamics were remarkably stable in all groups but required considerable fine tuning when enflurane was administered. The "stress" of CPB was blunted by the additional dose of sufentanil, as well as by enflurane. This was reflected in those patients receiving the extra sufentanil or enflurane by less severe increases in their epinephrine or norepinephrine concentrations and by less frequent use of sodium nitroprusside to control mean arterial pressure compared to the group of patients given the lower-dose sufentanil. This study suggests that higher blood levels of sufentanil can attenuate, but not eliminate, the stress response to CPB, as can enflurane, and that both the narcotic and inhalation anesthetic techniques for patients with coronary artery disease were quite satisfactory.

Anesthesia↗
PubMedDate not supplied

Recovery following general anesthesia with isoflurane or enflurane for outpatient dentistry and oral surgery.

Anesthesia was induced in 120 unpremedicated, healthy patients undergoing outpatient dentistry or oral surgery with methohexital, and endotracheal intubation facilitated with succinylcholine. Anesthesia was maintained randomly with either enflurane or isoflurane in nitrous oxide and oxygen (50%) administered in a nonrebreathing circuit using spontaneous respiration. After both enflurane and isoflurane anesthesia, it took 12-13 minutes before the patients were oriented as to time and place. The patients' ability to walk along a straight line normalized significantly (p < .05) more quickly after isoflurane than after enflurane anesthesia. Long enflurane anesthesia (>90 minutes) was associated with a significantly (p < .05-p < .01) slower recovery of walking ability and of psychomotor performance in a perceptual speed test than was short enflurane anesthesia (<40 minutes). With isoflurane the speed of recovery did not depend on the duration of anesthesia. After both anesthetic techniques, 25-26% of the patients had nausea or vomited. We conclude that using spontaneous respiration recovery is faster after isoflurane anesthesia than after enflurane anesthesia and that isoflurane should be preferred to enflurane for long anesthesia of outpatients.

Adult↗
PubMed1988

[The effects of isoflurane and enflurane on cerebral hemodynamics and cerebral oxygen consumption in humans].

The effects of isoflurane (1 MAC) and enflurane (1 MAC) on cerebral blood flow and cerebral oxygen consumption were studied in 20 male patients without intracranial disease undergoing coronary artery bypass surgery (mean age 57 and 59 years respectively). The aim of the study was to investigate whether both agents diminish autoregulation of cerebral blood flow and CO2 reactivity of cerebral blood vessels. Patients were randomly assigned to one of two groups (10 patients each) receiving either isoflurane 1.15 vol.% or enflurane 1.68 vol.% endexpiratory. Measurements were performed and blood samples were taken in the awake state (I); 15 min after achievement of steady-state conditions with 1.68 vol.% enflurane or 1.5 vol.% isoflurane without blood pressure support (II); during norepinephrine-induced hypertension at a cerebral perfusion pressure of 110 mmHg (III); and during controlled hyperventilation at a PaCO2 of 27 mmHg and normotension (IV). Cerebral blood flow was measured by the argon wash-in technique. Isoflurane and enflurane produced a significant drop in cardiac index and cerebral perfusion pressure and reduced cerebral blood flow significantly by 35% and 39% respectively. Cerebral oxygen consumption was also significantly decreased by 49% (isoflurane) and 50% (enflurane). Induced hypertension with norepinephrine increased cerebral blood flow significantly by 32% (isoflurane) and 26% (enflurane), while hypocapnia reduced cerebral blood flow significantly by 26% (isoflurane) and 29% (enflurane).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗