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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↗
PubMed2003

Interaction between artificial membranes and enflurane, a general volatile anesthetic: DPPC-enflurane interaction.

The structural modifications of the dipalmitoylphosphatidylcholine (DPPC) organization induced by increasing concentration of the volatile anesthetic enflurane have been studied by differential scanning calorimetry, small-angle, and wide-angle x-ray scattering. The interaction of enflurane with DPPC depends on at least two factors: the enflurane-to-lipid concentration ratio and the initial organization of the lipids. At 25 degrees C (gel state), the penetration of enflurane within the lipids induces the apparition of two different mixed lipid phases. At low anesthetic-to-lipid molar ratio, the smectic distance increases whereas the direction of the chain tilt changes from a tilt toward next-neighbors to a tilt between next-neighbors creating a new gel phase called L(beta')(2NNN). At high ratio, the smectic distance is much smaller than for the pure L(beta') DPPC phase, i.e., 50 A compared to 65 A, the aliphatic chains are perpendicular to the membrane and the fusion temperature of the phase is 33 degrees C. The electron profile of this phase that has been called L(beta)(i), indicates that the lipids are fully interdigitated. At 45 degrees C (fluid state), a new melted phase, called L(alpha)(2), was found, in which the smectic distance decreased compared to the initial pure L(alpha)(1) DPPC phase. The thermotropic behavior of the mixed phases has also been characterized by simultaneous x-ray scattering and differential scanning calorimetry measurements using the Microcalix calorimeter of our own. Finally, titration curves of enflurane effect in the mixed lipidic phase has been obtained by using the fluorescent lipid probe Laurdan. Measurements as a function of temperature or at constant temperature, i.e., 25 degrees C and 45 degrees C give, for the maximal effect, an enflurane-to-lipid ratio (M/M), within the membrane, of 1 and 2 for the L(alpha)(2) and the L(beta)(i) lamellar phase respectively. All the results taken together allowed to draw a pseudo-binary phase diagram of enflurane-dipalmitoylphosphatidylcholine in excess water.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1980

Baroreflex control of heart rate in man awake and during enflurane and enflurane--nitrous oxide anesthesia.

Baroreflex control of heart rate was assessed by means of a pressor test in two groups of subjects while awake and at two levels of anesthesia with enflurane (Group I) and enflurane-nitrous oxide (Group II). In the awake control situation, calculated mean slopes (+/- SD) were 23 +/- 8 (Group I) and 25 +/- 11 (Group II). There was no significant difference between the groups. During enflurane anesthesia (Group I) mean slopes were significantly depressed to 5 +/- 5 at 1 MAC and 6 +/- 6 at 0.8 MAC. During enflurane-nitrous oxide anesthesia (Group II), slopes were significantly depressed to 5 +/- 3 at 1 MAC and 6 +/- 4 at 0.9 MAC. There was no significant difference between the extents of depression in the two groups. It is concluded that both enflurane anesthesia and enflurane-nitrous oxide anesthesia at 1 MAC produce significant depression of baroreflex control of heart rate in man.

Adolescent↗
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↗
PubMed1980

Enflurane anesthesia in the pony: a comparative study between enflurane and halothane.

Enflurane, a new volatile anesthetic agent, was compared with halothane as components of a commonly used clinical anesthetic regime in the pony. Enflurane provides satisfactory general anesthesia when administered at a maintenance concentration of approximately 1.5-2.5%, in combination with a 1:1 nitrous oxide-oxygen mixture. With both agents cardiac rhythm and pulse were stable, however significant arterial hypotension occurred, especially during and following induction, being anesthetic concentration dependent. Hypoventilation was induced by both agents, there being no significant quantitative difference in respiratory depression despite significantly lower respiratory rates with enflurane. Serum electrolytes and liver enzymes did not change significantly with either regime. Emergence from anesthesia was smooth, and significantly more rapid with enflurance. Post-anesthetic complications were not observed with either agent.

Anesthesia, Inhalation↗
PubMed1982

The effect of acute elevation of blood pressure on myocardial performance during enflurane and enflurane with nitrous oxide anaesthesia in man.

Myocardial performance was assessed by a noninvasive method, when arterial pressure was raised acutely in eleven healthy subjects, awake and anaesthetized with equipotent (1 MAC) doses of either enflurane (Group 1) or enflurane with nitrous oxide 70 per cent. (Group 2). With anaesthesia, there was a significant and equal decrease in the indices of myocardial performance (p less than 0.05) in both groups with pressure elevation when compared to awake controls. The results are similar to those observed in subjects with depressed myocardial function due to either ischaemic heart disease or halothane anaesthesia.

Adolescent↗
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↗
PubMed1995

Stereoselective metabolism of enflurane by human liver cytochrome P450 2E1.

The toxicity of the chiral fluorinated volatile anesthetics halothane, enflurane, and isoflurane is closely related to their metabolism by hepatic cytochrome P450. Although individual anesthetic enantiomers have been shown to exhibit a difference in anesthetic efficacy, metabolism of anesthetic enantiomers has not been reported. Human liver enflurane metabolism to difluoromethoxydifluoroacetic acid (DFMDFA) and inorganic fluoride is catalyzed in vivo and in vitro by cytochrome P450 2E1. The purpose of this investigation was to characterize enflurane racemate and enantiomer metabolism to test the hypothesis that fluorinated ether anesthetic metabolism by cytochrome P450 2E1 exhibits substrate stereoselectivity. Enflurane metabolism by microsomes from three human livers and by microsomes containing cDNA-expressed human P450 2E1 was measured at saturating enflurane concentrations. DFMDFA was quantitated with gas chromatography-mass spectrometry by detection of the ethanolamide derivative. In microsomes from all three livers, (R)-enflurane metabolism was significantly greater than that of (S)-enflurane, whereas rates of racemic enflurane metabolism were generally between those seen for the R- and S-enantiomers. The ratio of (R)-enflurane to (S)-enflurane metabolism in the three livers studied was 2.1:1, 1.9:1, and 1.4:1. (R)-, (S)-, and racemic enflurane were all metabolized by expressed P450 2E1. The ratio of (R)-enflurane to (S)-enflurane metabolism was 1.9:1. The metabolic enantiomeric selectivity of human liver P450 2E1 for (R)-enflurane suggests that enflurane metabolism by P450 2E1 occurs by direct substrate oxidation, rather than indirectly through the generation of a P450-dependent reactive oxygen species, and supports the hypothesis that the P450 2E1 active site is somewhat restrictive and capable of stereochemical discrimination.

Anesthetics, Inhalation↗
PubMedDate not supplied

Porcine brain and myocardial perfusion during enflurane anesthesia without and with nitrous oxide.

Brain and myocardial blood flow (MBF) were examined in 10 previously instrumented swine during isocapnic conditions using 15 micron in diameter radionuclide-labeled microspheres that were injected into the left atrium. Minimum alveolar concentration (MAC) of enflurane required to prevent 50% of the pigs from responding by gross purposeful movement to a noxious stimulus was 1.66%. In pigs, 50% nitrous oxide decreased enflurane requirement for 1.0 MAC anesthesia by 0.82%. Each animal was studied during the following conditions: (a) unanesthetized (control); (b) 1.0 MAC enflurane anesthesia (1.66% end-tidal concentration); (c) 1.5 MAC (2.49%) enflurane anesthesia; (d) the equivalent of 1.0 and 1.5 MAC anesthesia produced by enflurane (0.84 and 1.67%) plus 50% nitrous oxide. Cerebral and total brain blood flow values were the same as control values during both levels of enflurane anesthesia. However, blood flow in the brainstem and cerebellum exhibited a dose-related increase; the increment of 28% for each of these regions at 1.5 MAC achieved statistical significance. Vascular resistance in all regions of the brain decreased with enflurane anesthesia. Substitution of 50% nitrous oxide for enflurane to maintain the same level of anesthesia markedly increased cerebral blood flow. At 1.0 and 1.5 MAC anesthesia produced using enflurane plus 50% nitrous oxide, cerebral blood flow was 151 and 183% of the control value, respectively. During enflurane plus nitrous oxide anesthesia equivalent to 1.5 MAC, cerebellar and brain stem blood flow were 135 and 180% of respective control values. MBF in all regions decreased in a dose-related manner with enflurane anesthesia. At 1.5 MAC enflurane, perfusion values in the walls of the left and the right ventricles were 52 and 59% of respective control values. During both levels of enflurane plus 50% nitrous oxide anesthesia, transmural MBF in all regions remained close to awake values. Subendocardial/subepicardial perfusion ration in both ventricles exceeded 1.00 during all steps of the protocol, thereby suggesting that subendocardial O2 delivery kept pace with O2 demand. These experiments have demonstrated that usage of 50% N2O with enflurane to produce equipotent anesthesia resulted in a dramatic increase in cerebral blood flow while MBF remained near awake value.

Anesthesia, Inhalation↗
PubMed1988

Interaction between diltiazem and halothane or enflurane in the canine blood-perfused papillary muscle and sinoatrial node preparations cross-circulated by chronically instrumented conscious donor dog.

Interaction of cardiovascular effects of diltiazem with those of halothane or enflurane was estimated in the canine isolated papillary muscle and sinoatrial node preparations perfused by arterial blood of the chronically instrumented conscious and halothane- or enflurane-anesthetized donor dog, into which diltiazem was infused i.v. at a rate of 20 micro g/kg/min for 60 min. One hour after diltiazem infusion, in the conscious donor dog, mean arterial pressure (MAP) and heart rate (DHR) were decreased to 84 +/- 3 and 84 +/- 2% and PQ interval (PQ) was prolonged to 148 +/- 5%, while in the isolated preparations, developed tension (DT) of the papillary muscle and sinoatrial rate (SAR) were decreased to 68 +/- 3 and 74 +/- 3% and blood flow (BF) was increased to 155 +/- 5% (n = 10). On the other hand, halothane (0.8%) anesthesia per se decreased MAP, DHR, DT and SAR to 89 +/- 8, 84 +/- 3, 79 +/- 3 and 89 +/- 5% (n = 7) of each basal value in conscious state 20 min after the inhalation. During halothane anesthesia, the same dose of diltiazem infused decreased MAP to 74 +/- 4 (n = 7), DHR to 66 +/- 4 (n = 6), DT to 62 +/- 7 (n = 7) and SAR to 69 +/- 1% (n = 3) of each value suppressed by halothane itself. Meanwhile, enflurane (1.7%) anesthesia itself decreased MAP, DHR, DT and SAR to 81 +/- 3, 85 +/- 2, 81 +/- 2 and 88 +/- 2% (n = 10) of each basal value in conscious state 30 min after enflurane inhalation. During enflurane anesthesia diltiazem decreased MAP to 74 +/- 3 (n = 10), DHR to 67 +/- 3 (n = 8), DT to 45 +/- 5 (n = 10) and SAR to 74 +/- 6% (n = 3) of each value under enflurane anesthesia alone. PQ interval of the donor dog heart was prolonged by halothane alone to 111 +/- 5% (n = 7) and by enflurane alone to 110 +/- 2% (n = 10) of the value before each anesthesia, and then diltiazem prolonged PQ interval to 160 +/- 8% (n = 6) and 174 +/- 10% (n = 8) of each value suppressed by the anesthetic itself during halothane- or enflurane-anesthesia, respectively. The second degree AV conduction block was induced in 1 of 7 halothane- and in 2 of 10 enflurane-anesthetized donor dogs, respectively. The sinus arrest was induced by diltiazem in 4 of 7 sinoatrial node preparations under halothane and in 7 of 10 ones during enflurane anesthesia. Moreover, plasma concentration of diltiazem 60 min after the start of infusion was 556 +/- 121 ng/ml in conscious dogs and tended to increase to 752 +/- 101 ng/ml in enflurane anesthetized donor dogs (n = 4), but there was no significant difference between two values (0.05 < P < 0.1). These results indicate that effects of diltiazem could be potentiated during halothane or enflurane anesthesia by elimination of compensatory reflex noted in conscious state, and that the negative inotropic effect of diltiazem was enhanced by enflurane anesthesia due to unknown mechanisms which probably include a slight but insignificant increase in plasma concentration.

Journal Article↗
PubMed1996

The direct effects of enflurane on coronary blood flow, myocardial oxygen consumption, and myocardial segmental shortening in in situ canine hearts.

This study evaluated changes in coronary blood flow (CBF), myocardial oxygen consumption (MVo2), and myocardial segmental shortening (SS) during intracoronary administrations of enflurane in in situ canine hearts. The left anterior descending coronary artery (LAD) of 11 anesthetized and mechanically ventilated dogs was perfused at constant perfusion pressure (80 mm Hg) with enflurane-free blood or with blood equilibrated in an extracorporeal oxygenator with enflurane (1.1%, 2.2%, 4.4%). CBF (measured with a Doppler flow transducer) was multiplied by the local arteriovenous (A-V) O2 difference to calculate MVo2. SS was measured with ultrasonic crystals. Myocardial lactate uptake was assessed. Peak CBF responses during enflurane were compared with those during maximum coronary vasodilation with adenosine. Enflurane caused concentration-dependent increases in CBF, and decreases in MVo2 and SS. The greatest increase in CBF during enflurane (4.4%) was similar to that achievable with adenosine. Myocardial lactate uptake was not affected by enflurane. In conclusion, enflurane has a direct coronary vasodilating effect. The potency of this effect is underscored by the ability of enflurane to cause marked increases in CBF, while appreciably reducing myocardial O2 demand. Since the enflurane-induced reduction in myocardial contractility was not due to ischemia, it likely reflected a direct negative inotropic effect. When the direct effects of enflurane are compared with those of equianesthetic concentrations of halothane and isoflurane previously shown in the same model, enflurane has a coronary vasodilating effect similar to that of halothane but less than that of isoflurane, and it has a negative inotropic effect greater than that of both isoflurane and halothane.

Anesthetics, Inhalation↗
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↗
PubMed1994

Mechanisms of action of enflurane on vascular smooth muscle. Comparison of rabbit aorta and femoral artery.

BACKGROUND: This study was performed to elucidate the mechanisms of action of enflurane by comparing the vascular smooth muscle responses of conduit arteries of larger (aorta) and smaller (femoral artery) diameter to enflurane using isolated rings and skinned strips. METHODS: Isolated intact rings (endothelium denuded) of aorta and femoral artery from rabbits were activated by various concentrations of norepinephrine (NE) and the effects of enflurane were examined at the steady-state force. In a separate study, the rings were pretreated with verapamil before the NE activation and tested with enflurane. In the saponin-treated arterial strips ("skinned"), the effects of enflurane on Ca2+ uptake or release from the sarcoplasmic reticulum were studied using caffeine-induced tension transients. RESULTS: In isolated aortic rings, enflurane (0.9%-5%) enhanced tension development at low NE concentrations (5 and 30 nM) but depressed it at highest concentration (10 microM). In contrast, enflurane depressed tension development in the femoral artery at all NE concentrations. Enflurane caused significant increase in the NE-activated force in rings pretreated with verapamil. In skinned strips, enflurane (1%-3%) decreased Ca2+ uptake (concentration resulting in 50% depression: 1.8% for aorta and 2.5% for femoral artery) and increased Ca2+ release from the sarcoplasmic reticulum (59%-208% for aorta and 10%-55% for femoral artery). These effects were dose-dependent. Enflurane potentiated ryanodine depression of caffeine-induced tension transients. CONCLUSIONS: Enflurane has similar mechanisms of action in aorta and femoral artery: blocking Ca2+ influx, and causing, at least in part, Ca2+ release from the sarcoplasmic reticulum through the ryanodine-receptor channel. These cellular actions of enflurane account for the depression in femoral artery and enhancement in aorta of NE-activated force in isolated rings.

Animals↗
PubMed1984

Effects of enflurane on coronary haemodynamics in patients with ischaemic heart disease.

The effects of enflurane with and without nitrous oxide on coronary haemodynamics and myocardial oxygenation were investigated in 11 patients with generalised atherosclerotic disease. Enflurane decreased systemic blood pressure (-50%) mainly by systemic vasodilation (SVR -41%) and to a lesser degree by impairment of cardiac performance (CO -27%). A change from 1MAC enflurane-nitrogen-oxygen (70/30) to 1MAC enflurane-nitrous oxide-oxygen (70/30) decreased blood pressure and cardiac output further (-16% and -14%). Enflurane-nitrogen-oxygen decreased coronary blood flow (-29%) and perfusion pressure (-47%). Coronary vascular resistance fell (-20%) along with decreases in myocardial oxygen consumption and extraction (-40% and -16%). Regional coronary blood flow measurements in four of the patients revealed maldistribution of blood flow. During enflurane-nitrous oxide-oxygen, myocardial oxygen consumption and extraction decreased further (-29% and -12%) without change in coronary blood flow or resistance. Myocardial ischaemia was observed in four patients during enflurane-nitrogen. During enflurane-nitrous oxide, ischaemia disappeared in two of the previously ischaemic patients and appeared in two not previously ischaemic. The regional blood flow maldistribution was abolished with nitrous oxide. It is concluded that enflurane is a powerful coronary vasodilator and in this respect slightly less potent than isoflurane. Enflurane may induce myocardial ischaemia by redistributing coronary blood flow and/or by producing hypotension. Nitrous oxide added to enflurane depresses cardiac function and augments the coronary vasodilatory effect of enflurane to a level at which coronary blood flow becomes totally pressure dependent.

Aged↗