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At least 19 recordsLinked to original sources
PubMed1989

Absence of agonistic or antagonistic effect of flumazenil (Ro 15-1788) in dogs anesthetized with enflurane, isoflurane, or fentanyl-enflurane.

This study determined the effects of flumazenil on the anesthetic requirements (MAC) of the dog for isoflurane (group 1; n = 6), enflurane (group 2; n = 7), and a combination of fentanyl-enflurane (group 3; n = 6). Control MAC in each group was determined by the tail-clamp method. Each animal in groups 1 and 2 received four iv incremental doses of flumazenil: 0.5, 1.0, 1.5, and 4.5 mg/kg, and isoflurane MAC or enflurane MAC was determined after each dose. The animals in group 3 received a loading dose and a continuous infusion of fentanyl 0.8 micrograms.kg-1.min-1 over 8 h, and enflurane MAC was determined four times during this experimental period. After the fourth enflurane MAC determination in each animal of group 3, a single iv dose of flumazenil 1.5 mg/kg was injected and enflurane MAC was then determined for the last time. In the incremental doses administered, flumazenil did not demonstrate any agonistic or antagonistic interaction with isoflurane, enflurane, or the fentanyl-enflurane combination. In group 3, plasma fentanyl concentrations remained stable at 12.5 +/- 3.0 ng/ml (mean +/- SD) throughout the experiment and reduced enflurane MAC by 60 +/- 8%. The addition of flumazenil changed neither the fentanyl concentration in plasma (12.2 +/- 3.8 ng/ml) nor its reduction of enflurane MAC (61 +/- 7%). In conclusion, the absence of effect of flumazenil on the MAC of enflurane, isoflurane, or a fentanyl-enflurane combination suggests that they do not interact with the benzodiazepine receptor.

Anesthesia, Intravenous↗
PubMedDate not supplied

Potential metabolic basis for enflurane hepatitis and the apparent cross-sensitization between enflurane and halothane.

Clinical case reports of unexplained hepatic dysfunction following enflurane and isoflurane anesthesia led to the hypothesis that oxidative metabolism of these drugs by cytochromes P-450 produces immunoreactive, covalently bound acylated protein adducts similar to those implicated in the genesis of halothane-induced hepatic necrosis. Microsomal adducts were detected by enzyme-linked immunosorbent assay and immunoblotting techniques utilizing specific anti-trifluoroacetyl (TFA) IgG hapten antibodies in rat liver following enflurane, isoflurane, or halothane administration. Preincubation of the antibodies with microsomes from halothane-pretreated rats or with 500 microM TFA-lysine, markedly inhibited adduct recognition, while preincubation with 500 microM acetyllysine had no effect. The relative amounts of immunoreactive protein adducts formed were halothane much greater than enflurane much greater than isoflurane and correlates directly with the relative extents of metabolism of these agents. These results support the view that acyl metabolites of the volatile anesthetics may become covalently bound to hepatic proteins, thus serving as antigens, and thereby account for the apparent cross-sensitization and idiosyncratic hepatotoxicity reported for these drugs.

Acylation↗
PubMed1992

[Plasma catecholamine levels during air-oxygen-enflurane anesthesia compared with those during nitrous oxide-oxygen-enflurane anesthesia].

This study was designed to investigate the differences in plasma levels of epinephrine, norepinephrine and dopamine during air-oxygen-enflurane anesthesia (AOE) and those during nitrous oxide-oxygen-enflurane anesthesia (GOE). These catecholamine levels were measured at 8 carefully defined points before and during hysterectomy or ovariectomy in two groups of each ten patients. Plasma levels of epinephrine decreased significantly immediately after intubation in both groups. In the AOE group, epinephrine levels increased significantly 30 and 60 minutes after the beginning of the operation. In the GOE group, however, epinephrine levels decreased significantly 15 and 30 minutes after the beginning of the operation. The difference between the two groups was statistically significant. Plasma levels of norepinephrine increased significantly after the beginning of the operation in the GOE group but no significant differences were found in the AOE group except the levels 60 minutes after the operation. The difference between the two groups was statistically significant 15 minutes after the operation. Plasma levels of dopamine remained unchanged in the two groups. Mean arterial pressure changed with intubation and surgical stress in the two groups. The arterial pressure was significantly higher 30 minutes after the operation in the GOE group compared with AOE group. Pulse rate increased significantly during anesthesia and surgery in the GOE group. It is concluded that AOE induces more increase of plasma epinephrine and less release of plasma norepinephrine compared with GOE.

Adult↗
PubMed1991

Effects of augmenting cardiac contractility, preload, and heart rate on cardiac output during enflurane anesthesia.

Changes in cardiac output in response to augmenting cardiac contractility, preload, and heart rate during enflurane anesthesia were examined in 12 open-chested dogs. Cardiac contractility was assessed by the slope of the end-systolic pressure-volume relation (Emax). Dobutamine (3, 6, and 9 micrograms.kg-1.min-1) was administered to augment cardiac contractility. Autologous blood (5.0 and 10 mL/kg) was infused to increase preload. Atrial pacing was used to increase the heart rate by about 30%. Cardiac output decreased from 96 +/- 4 (0% enflurane) (mean +/- SE) to 73 +/- 5 (1.7% enflurane) and to 46 +/- 7 mL.kg-1.min-1 (3.4% enflurane), concomitantly with decreases in Emax from 6.0 +/- 1.2 (0% enflurane) to 4.5 +/- 1.2 (1.7% enflurane) and to 2.5 +/- 0.5 mm Hg/mL (3.4% enflurane). Dobutamine (3, 6, and 9 micrograms.kg-1.min-1) increased Emax from 69% +/- 7% (compared to 0% enflurane with no dobutamine) to 139% +/- 15%, 167% +/- 25%, and 183% +/- 35% at 1.7% enflurane, and from 43% +/- 8% to 78% +/- 7%, 137% +/- 20%, and 157% +/- 22% at 3.4% enflurane, respectively. The decreases in cardiac output by 1.7% and 3.4% enflurane were reversed by the intravenous administration of 3 micrograms.kg-1.min-1 of dobutamine. Cardiac output was significantly increased by administration of 10 mL/kg of autologous blood at 1.7% enflurane, but did not significantly increase at 3.4% enflurane. Increasing the heart rate did not significantly increase cardiac output at 1.7% and 3.4% enflurane. The results of this study suggest that increasing cardiac contractility is the most effective therapeutic means of reversing circulatory depression during enflurane anesthesia.

Anesthesia↗
PubMed1988

Metabolic activation of intercortical and corticothalamic pathways during enflurane anesthesia in rats.

The purpose of this study was to examine the effects of enflurane on local cerebral glucose utilization (LCGU), and to provide further insight into the mechanism of the epileptogenic properties of enflurane. Twenty-four male Wistar rats were divided into four groups; three groups with intact cortex received 0.5, 2, or 4% enflurane, and one group with unilateral cortex excised received 4% enflurane. LCGU was measured at each anesthetic concentration using the autoradiographic 2-[14C]deoxyglucose method. LCGU in ten of 33 structures examined during 2% enflurane decreased by 19-33%, and LCGU in 22 structures during 4% enflurane decreased by 19-65%, when compared with that during 0.5% enflurane. While LCGU, in most structures, decreased in a dose-related manner, LCGU in the corpus callosum, thalamic ventrobasal complex, and hippocampal CA3 field during 4% enflurane increased by 31-70%, compared with that during 0.5% and/or 2% enflurane. With unilateral cortical excision during 4% enflurane, the increase in LCGU in the ventrobasal complex was obliterated in the excision side, and the increase in the corpus callosum was attenuated. High LCGU in the hippocampal CA3 field and contralateral ventrobasal complex was not affected with cortical excision. These results indicate that intercortical and corticothalamic pathways are metabolically activated during deep enflurane anesthesia, suggesting that the epileptogenic property of enflurane is related to activation of these pathways.

Anesthesia, Inhalation↗
PubMed1986

Thiopental and epinephrine-induced dysrhythmias in dogs anesthetized with enflurane or isoflurane.

Epinephrine-induced dysrhythmias were studied in 19 dogs anesthetized with 1.25 MAC enflurane or isoflurane, or the same preceded by thiopental (20 mg/kg). In 11 (group 1) dogs, thiopental reduced the dose of epinephrine required for production of ventricular ectopy, bigeminy and tachycardia with enflurane, and only ventricular tachycardia with isoflurane (P less than 0.05). Thiopental potentiation of epinephrine-induced dysrhythmias with enflurane lasted 4 hr after induction. In eight (group 2) dogs, the arrhythmic dose (ADE in microgram/ml) and plasma level of epinephrine (PLE in ng/ml) for four or more ventricular extrasystoles in 15 sec were determined in the same animal under each of the four test conditions. ADE and PLE values (X +/- SEM) were, respectively, enflurane, 9.1 +/- 1.0 and 141 +/- 24 (8/8 dogs); enflurane-thiopental, 5.0 +/- 0.6 and 63 +/- 16 (8/8 dogs); isoflurane, 28.3 and 330 (1/7 dogs); and isoflurane-thiopental, 15.2 +/- 2.8 and 265 +/- 59 (5/7 dogs). In addition, thiopental had no effect on plasma epinephrine levels reached during epinephrine infusions with 1.0 (enflurane only), 2.0 (enflurane, isoflurane) and 4.0 micrograms X kg-1 X min-1 (isoflurane only). Nor were epinephrine levels reached during enflurane or enflurane-thiopental different from those reached during isoflurane or isoflurane-thiopental. It is concluded that thiopental potentiates several types of epinephrine-induced ventricular dysrhythmias with enflurane, but only ventricular tachycardia with isoflurane. Furthermore, isoflurane or isoflurane-thiopental were less sensitizing than enflurane or enflurane-thiopental. Finally, neither thiopental nor the anesthetic agents affected plasma epinephrine levels reached during epinephrine infusions lasting 3 min.

Animals↗
PubMed1989

The nonlinear contribution of nitrous oxide at sub-MAC concentrations to enflurane MAC in rats.

The presumed linear relationship describing the contribution of nitrous oxide (N2O) to the enflurane requirement necessary to achieve a 1.0 MAC level of anesthesia was tested in rats (N = 84). Each rat received one of six different concentrations of N2O, and enflurane was adjusted to attain 1.0 MAC with the use of a standard tail clamp method. The resultant group MAC anesthetic concentrations were Group I-N2O = 0.0%, enflurane = 2.30%; Group II-N2O = 10.4%, enflurane = 2.19%; Group III-N2O = 30.7%, enflurane = 1.85%; Group IV-N2O = 61.8%, enflurane = 1.75%; Group V-N2O = 70.9%, enflurane = 1.56%; and Group VI-N2O = 80.3%, enflurane = 1.54%. Increasing the N2O concentration from 0-10%, from 30-60%, or 70-80% did not significantly decrease the enflurane requirement; however, increasing the N2O concentration from 10-30% or 60-70% produced a significant decrease (P less than 0.05) in the concentration of enflurane required for 1.0 MAC of anesthesia. Thus, in rats, increasing the concentration of N2O in sub-MAC ranges did not produce a linear decrease in the enflurane concentration required to add up to 1.0 MAC of anesthesia. These results are consistent with a dose-dependent interaction between N2O and the excitatory properties of enflurane; this interaction could represent synergism at low concentrations or antagonism at higher concentration of N2O.

Animals↗
PubMed1990

Edrophonium antagonism of atracurium during enflurane anaesthesia.

To determine the influence of enflurane on the ability of edrophonium to antagonize atracurium block, dose-response curves were constructed for edrophonium in the presence of 0%, 1% and 2% enflurane, and for 2% enflurane discontinued at the time of administration of edrophonium. One hundred ASA Physical Status I or II patients (four groups of 25), selected randomly and undergoing elective surgery, received atracurium 0.5 mg kg-1, with thiopentone, nitrous oxide and enflurane. Supplementary doses of fentanyl were given if needed. Train-of-four (TOF) stimulation was applied every 12 s, and the force of contraction of the adductor pollicis muscle was recorded. When first twitch height (T1) had recovered spontaneously to 10% of initial value, edrophonium 0.1, 0.2, 0.4 or 1 mg kg-1 was administered by random allocation. Enflurane concentrations remained constant, except that enflurane was discontinued in 50% of the patients who had received 2% enflurane. Monitoring was continued for at least 10 min, at which time T1 and TOF ratio (T4/T1) were measured. The ED80 for T1 recovery depended on the dose of enflurane: 0.08 (SEM 0.03), 0.21 (0.06) and 0.42 (0.18) mg kg-1 for 0%, 1% and 2% enflurane, respectively (P less than 0.005). With enflurane 2% discontinued, the ED80 was 0.095 (0.050) mg kg-1 (P less than 0.02 compared with 2% enflurane).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Less than additive antinociceptive interaction between midazolam and fentanyl in enflurane-anesthetized dogs.

The anesthetic interactions of midazolam and fentanyl were determined in terms of enflurane MAC reduction in dogs. In part 1, 8 animals received an intravenous (iv) loading dose of fentanyl followed by a constant infusion at 0.05 micrograms.kg-1.min-1 to produce a stable enflurane MAC reduction of approximately 20%. Midazolam was then administered in a series of three incremental loading doses and infusions (2.4, 9.6, and 28.8 micrograms.kg-1.min-1 previously determined to produce enflurane MAC reductions of approximately 30, 45, and 60%, respectively. Enflurane MAC was determined for each infusion. Then fentanyl was discontinued; naloxone 1 mg/kg was administered; and enflurane MAC was determined. In part 2, six dogs received a loading dose and a continuous infusion of fentanyl (0.2 micrograms.kg-1.min-1) designed to produce a stable enflurane MAC reduction of approximately 40%. A series of two incremental loading doses and infusions of midazolam (2.4 and 28.8 micrograms.kg-1.min-1) were added, and MAC determinations were repeated at each infusion rate. Then midazolam was discontinued; flumazenil (RO 15-1788) 1.5 mg/kg was administered; and enflurane MAC was determined. The fentanyl concentrations in plasma remained stable at 1.0 +/- 0.3 ng/ml (mean +/- standard deviation [SD], part 1) and 3.1 +/- 0.5 ng/ml (part 2) throughout the study and, in the absence of midazolam, reduced enflurane MAC by 28 +/- 11 and 44 +/- 5%, respectively. The addition of midazolam produced significant further reductions in enflurane MAC, but the reductions were less than those predicted on the basis of an additive interaction. Naloxone returned enflurane MAC reduction to that expected for midazolam alone (part 1).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1992

Enflurane-induced release of an excitatory amino acid, glutamate, from mouse brain synaptosomes.

To clarify the mechanisms of enflurane-induced convulsions, we examined the effects of enflurane, halothane, and diethyl ether on the release of an excitatory neurotransmitter, glutamate, from isolated pinched-off nerve terminals (synaptosomes) of the mouse cerebral cortex. At concentrations corresponding to those used clinically (0.75 and 1.25 mM), enflurane released more glutamate than did halothane. Diethyl ether (10 and 58 mM) had no effect on glutamate release. Enflurane (0.75-15 mM) increased glutamate and aspartate release in a dose-dependent manner but had little effect on the release of the inhibitory neurotransmitters glycine and gamma-aminobutyric acid or on the release of glutamine. A glutamate uptake inhibitor, kainic acid (1 mM), did not affect enflurane-induced glutamate release. Replacement of the medium's Ca2+ by Co2+, or exposure to cold (about 2 degrees C), suppressed the enflurane-induced glutamate release. Depolarization caused by 40 mM K+ increased the basal level of glutamate released, and enflurane-induced glutamate release was lower after depolarization. Enflurane had no effect in synaptosomes prepared from the cerebellum, diencephalon and pons, or medulla oblongata. Thus, enflurane increased Ca(2+)- and temperature-dependent glutamate release, especially from synaptosomes of the cerebral cortex. These data provide a pathophysiologic explanation for enflurane-induced convulsions.

Animals↗
PubMed1988

Pharmacokinetics and pharmacodynamics of midazolam in the enflurane-anesthetized dog.

Midazolam (Mid) is widely used as an anesthetic adjunct. To test its anesthetic effect vs. concentration relationships, it is desirable to establish stable and predictable Mid concentrations in plasma (and brain). Therefore, the pharmacokinetics of Mid in the enflurane-anesthetized dog were determined, and the ability of Mid to reduce the enflurane concentration required for anesthesia was measured and correlated with the Mid concentration in plasma [MID]. Mongrel dogs (n = 9) were anesthetized with enflurane and the enflurane EC50 (MAC--the end-tidal concentration at which one-half of the dogs respond to the noxious stimulation of clamping of the tail, and one-half do not) was determined. Group 1 (n = 5) received Mid 2.5 mg/kg iv over 60 sec. Plasma for determination of [MID] was collected and the enflurane EC50 was determined repeatedly over the 7-8-hr period following injection. Based on the pharmacokinetic parameters determined for Group 1, dogs in Group 2 (n = 4) received Mid as a continuous infusion of 21 micrograms kg-1 min-1 for 5 hr accompanied by an initial loading dose (3 mg/kg infused over 20 min) designed to produce a stable [MID] of 1000 ng/ml in plasma. Enflurane MAC and [MID] were determined regularly during the infusion and for 6 hr after discontinuation of the infusion. There were no important differences in the pharmacokinetic parameters determined for Group 1 vs. Group 2: t1/2,z = 98 +/- 5 vs. 95 +/- 10 min (mean +/- SEM); V = 3.94 +/- 0.27 vs. 2.98 +/- 25 L/kg; Cl = 28.5 +/- 3.1 vs. 22.3 +/- 1.1 ml kg-1 min-1, respectively. When administered as a continuous intravenous infusion (Group 2), [MID] remained stable at 949 +/- 53 ng/ml for more than 5 hr. The enflurane EC50 was reduced by 55% and the reduction remained stable during the 5 hours of Mid infusion. After a single iv bolus dose or after discontinuation of the continuous infusion, the degree of enflurane EC50 reduction diminished toward the control (i.e., enflurane alone) value as [MID] declined. Mid-azolam's pharmacokinetics and plasma concentration vs. effect relationships have been determined to be consistent under two different experimental conditions.

Anesthesia, General↗
PubMed1989

Myocardial contractility, blood flow, and oxygen consumption in healthy dogs during anesthesia with isoflurane or enflurane.

Left ventricular contractility (Vmax), myocardial blood flow (MBF), and oxygen consumption (O2C) were determined together with systemic hemodynamic parameters in a total of 21 mongrel dogs. Baseline recordings were obtained under basal anesthetic conditions with a narcotic (piritramid, IV). In the control group (n = 7), recordings were obtained during a three-hour observation period with infusion of piritramid. In experimental groups measurements were repeated with equi-anesthetic concentrations of isoflurane (0.7 and 1.4 vol%; n = 8) and enflurane (1.1 and 2.2 vol%; n = 6). Dose-dependent reductions of arterial pressure, cardiac output (CO) and peripheral vascular resistance were observed with isoflurane and enflurane. CO at the higher anesthetic level was depressed significantly more with enflurane. This difference was obviously due to a more severe depression of myocardial contractility with enflurane; Vmax was decreased by 18% and 26% with enflurane, but only by 10% and 17% with isoflurane (P less than 0.01). MBF and the fraction of CO received by the heart were increased above their baseline values with both concentrations of isoflurane. In contrast, the fraction of CO remained constant with enflurane while MBF decreased. O2C was reduced due to decreases of afterload and left ventricular contractility. The reduction was greater with enflurane than with isoflurane. All parameters remained unchanged in the control group. The results of this study indicate that the most striking difference in the actions of isoflurane and enflurane on cardiac parameters is on myocardial vascular resistance; MBF is increased with isoflurane, but is decreased with enflurane although myocardial perfusion pressure is reduced by almost identical amounts.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1989

Pretreatment with paracetamol inhibits metabolism of enflurane in rats.

We studied the interaction between paracetamol (acetaminophen U.S.P.) and enflurane. Sixteen rats were assigned to four groups (n = 4) to receive: paracetamol 7.5 mg/100 g body weight; paracetamol plus 1% enflurane; 1% enflurane alone, or no treatment (controls). Animals were killed 6 h later. A second series of 16 were treated identically, but were killed after 24 h. Measurements were made of fluoride concentrations in serum, liver and urine (indicators of biotransformation of enflurane), paracetamol concentrations in urine, pathological changes in liver samples, and concentrations of the enzymes aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum. Pretreatment with paracetamol significantly decreased urinary fluoride at 6 and 24 h after exposure to enflurane, but decreased fluoride concentrations in serum and liver only at 6 h after exposure to enflurane. Paracetamol concentrations in urine did not change after exposure to enflurane. Exposure to paracetamol alone increased AST and ALT. At 24 h after exposure to enflurane, serum concentrations of enzymes in rats pretreated with paracetamol were similar to those of control rats. Pretreatment with paracetamol may therefore inhibit metabolism of enflurane. Although no hepatic damage was observed, the increased in AST and ALT suggested subclinical liver damage in rats given only paracetamol.

Acetaminophen↗
PubMed1989

Ethanol-inducible cytochrome P450 in rabbits metabolizes enflurane.

Following anaesthesia with enflurane, some patients receiving isoniazid have increased serum concentrations of fluoride ion, presumably because of induction of an isozyme of cytochrome P450 which is responsible for enflurane biodegradation. In rats, isoniazid and ethanol enhance metabolism of enflurane and also induce a form of cytochrome P450 which is homologous with a form of rabbit liver cytochrome P450 known as 3a. Isoniazid, ethanol and imidazole increase the concentration of cytochrome P450 3a in hepatic microsomes. We have pretreated rabbits with imidazole, the most potent of the three inducers of isozyme 3a, to determine if the hepatic microsomal metabolism of enflurane is enhanced and if purified isozyme 3a catalyses the oxidation of enflurane. Imidazole produced a 250% increase in the hepatic microsomal metabolism of enflurane, sevoflurane, methoxyflurane and the control substrate, aniline. Polyclonal antibodies to cytochrome P450 3a inhibited 90% of enflurane metabolism, but only 40% of methoxyflurane biotransformation in the microsomes from imidazole-pretreated rabbits. Thus isozyme 3a or a structurally similar cytochrome P450 seemed to catalyse almost all microsomal metabolism of enflurane. In addition, purified cytochrome P450 3a catalysed the metabolism of enflurane, sevoflurane and methoxyflurane, and the oxidation of these anaesthetics by cytochrome P450 3a was stimulated four-fold by cytochrome b5, a protein which serves as an alternate source of electrons for some cytochrome P450 reactions.

Anesthetics↗
PubMed1989

Different 1.2 MAC combinations of nitrous oxide-enflurane cause unique cerebral and spinal cord metabolic responses in the rat.

The effect of three different 1.2 MAC combinations of nitrous oxide (N2O) and enflurane upon glucose metabolism in the central nervous system was evaluated in male rats (n = 30). Anesthesia was induced with enflurane and N2O prior to tracheal intubation and mechanical ventilation. Physiologic variables (temperature, blood pressure, pH, PaO2, PaCO2, serum glucose, and hematocrit) were maintained within normal limits. Each rat was randomly assigned one of the following 1.2 MAC anesthetic regimens: 1) control--0% N2O/2.76% enflurane, 2) treatment 1--30% N2O/2.26% enflurane, or 3) treatment II--60% N2O/2.12% enflurane. Following anesthetic equilibration, an autoradiographic evaluation of local cerebral and spinal cord glucose utilization was performed. There were no differences in the physiologic data. As enflurane was partially replaced by an equivalent MAC fraction of N2O (0-30%), a heterogeneous activation of cerebral metabolism was observed in selected sensory input structures, and in components of the limbic system. The values tended to return to control when N2O was increased to 60% (and the enflurane was appropriately reduced). At all spinal cord levels, a homogeneous increase in metabolism was observed in both white and grey matter when enflurane was replaced by the 0-30% N2O change, with a return to control when the N2O was further increased from 30-60%. Thus, in rats, increasing the N2O concentration (while concurrently decreasing enflurane) produced a biphasic metabolic response. Metabolism was activated when N2O was increased from 0-30%, with a relative depression in metabolism when N2O was further increased from 30-60%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Nitrous oxide increases enflurane concentrations delivered by Ethrane vaporizers.

Delivered enflurane concentrations from two calibrated Ethrane vaporizers were determined with total gas flows of 3,5 and 8 L/min. Regardless of total gas flow the presence of 60% nitrous oxide increased enflurane concentrations by 20 to 40% above those concentrations present when only oxygen was flowing through the vaporizer. This nitrous oxide effect was present at all dial settings studied except the lowest engraved (0.25) concentration. Enflurane output at the 0.25% setting was 0.38% with or without nitrous oxide. Maximum changes in enflurane concentrations after adding nitrous oxide required about 5 minutes but the rapidity with which enflurane concentrations approached this maximum value were directly related to total gas flow. Similar effects of nitrous oxide on enflurane output from Cyprane Ethrane vaporizers were also measured. The mechanism of increased vaporizer enflurane output in the presence of nitrous oxide is unknown but may reflect increased gas flow through the vaporizing chamber secondary to increase in gas density associated with nitrous oxide. A similar mechanism has been proposed to explain increased halothane concentrations delivered by Fluotec Mark 2 vaporizers in the presence of nitrous oxide. Clinically, central system stimulation and anesthetic overdose may occur from increased enflurane concentrations delivered when nitrous oxide is added to the gases flowing through the Ethrane vaporizer. The ability to deliver low enflurane concentrations is limited since the measured concentration at the lowest dial setting was nearly 0.4%.

Anesthesia, Inhalation↗
PubMed1990

Different effects of halothane and enflurane on diaphragmatic contractility in vivo.

We examined the effects of halothane and enflurane on diaphragmatic contractility in 12 anesthetized, mechanically ventilated dogs. The diaphragmatic force was assessed from transdiaphragmatic pressure (Pdi) developed at functional residual capacity against an occluded airway during cervical phrenic nerve stimulation. Animals were randomly assigned to two groups, a halothane group (n = 6) and an enflurane group (n = 6). The Pdi stimulus-frequency relationship was compared at anesthetic levels of 1, 1.5, and 2 MAC (minimum alveolar concentration) in each group. The sequence of changing anesthetic concentration was randomized. In addition, the Pdi-frequency relationship was also compared between 1 MAC of halothane and enflurane in 8 of 12 dogs. In animals anesthetized with enflurane, Pdi significantly decreased with 50- and 100-Hz stimulation in the presence of increasing MAC values, whereas Pdi at 10-Hz stimulation was not affected by the depth of anesthesia. Pdi with 20-Hz stimulation during 2 MAC enflurane also decreased significantly below Pdi levels seen at 1 and 1.5 MAC. By contrast, with halothane there was no difference in Pdi at any of the stimulation frequencies during any of the three levels of anesthesia. There was no statistical difference, however, between Pdi-frequency relationships during 1 MAC of halothane and enflurane in eight animals. From these results, we conclude that halothane does not impair diaphragmatic contractility any more than enflurane does, but enflurane decreases force generation of the diaphragm at high stimulation frequencies in a dose-related fashion. This depressant effect of enflurane occurs mainly through the impairment of neuromuscular transmission and/or membrane excitability.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗