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PubMed1989

Randomized comparison of outcome after propofol-nitrous oxide or enflurane-nitrous oxide anaesthesia in operations of long duration.

A randomized, prospective, comparative study was performed to evaluate induction characteristics, haemodynamic changes and recovery in 60 ASA I-II patients undergoing mainly gynaecological laparotomies with either propofol or thiopentone-enflurane anaesthesia. The propofol group (n = 30) received 2 mg.kg-1 propofol for induction of anaesthesia followed by propofol infusion. The thiopentone-enflurane group (n = 30) received thiopentone 4 mg.kg-1 for induction followed by enflurane (0.5-2 per cent). All patients received nitrous oxide (66 per cent] in oxygen begun one minute after tracheal intubation, and fentanyl (1.5 micrograms.kg-1) four minutes prior to induction. Other drugs administered during or after anaesthesia were similar among the groups. Haemodynamic measurements were similar between propofol and enflurane groups except after tracheal intubation when the mean arterial pressure was lower in the propofol group (P less than 0.05). The propofol group had significantly less (P less than 0.01) emesis in the recovery room than the enflurane group. The propofol group experienced significantly less (P less than 0.05) dizziness, depression/sadness and hunger than the enflurane group in the postoperative period as assessed with a visual analogue questionnaire. We conclude that propofol provided better outcome than enflurane in terms of these nonvital but annoying outcome measures after relatively long intra-abdominal operations.

Adult↗
PubMed1982

Effect of enflurane and fentanyl on the clinical characteristics of long-term succinylcholine infusion.

The characteristics of the neuromuscular block produced by prolonged succinylcholine infusion were compared in 40 patients anaesthetized with either nitrous oxide with enflurane (1-2 per cent inspired) or nitrous oxide and fentanyl. Neuromuscular transmission was monitored using train-of-four stimulation and the infusion rate was adjusted to keep the first twitch at 10-15 per cent of its control value. Initially, all patients, exhibited a depolarizing-type block all twitches of the train-of-four being roughly the same size, and the infusion rates were similar in the enflurane (54 microgram X kg-1/min) and the fentanyl (58 microgram X kg-1/min) groups. Tachyphylaxis developed later in both groups and correlated well with the onset of phase II block (dual block). This occurred sooner and at a lower cumulative dose in the enflurane group. Fourth to first twitch ratios decreased to 50, 25 and 0 per cent in 31, 46 and 59 minutes in the enflurane group, at cumulative succinylcholine doses of 2.2, 3.2 and 4.2 mg X kg-1 respectively. Corresponding figures for the fentanyl group were 52, 73 and 86 minutes, with dose of 3.4, 5.0 and 5.9 mg X kg-1. Infusion rates increased markedly after establishment of dual block, but were similar with enflurane (0.99 mg X kg-1/min) and fentanyl (1.12 mg X kg-1/min). Ten minutes after stopping the infusion fourth to first twitch ratios failed to reach 50 per cent in most patients given enflurane who had received more than 6 mg X kg-1 succinylcholine over more than 90 minutes. Corresponding figures for fentanyl patients were 13 mg x kg-1 and 150 minutes. The block in all 15 patients (9 enflurane, 6 fentanyl) who did not recover spontaneously was successfully antagonized with atropine and neostigmine.

Adult↗
PubMed1990

Effects of enflurane on 5-hydroxytryptamine transport in synaptosomes from rat brain.

The administration of volatile anesthetics to laboratory animals has been reported to alter brain 5-hydroxytryptamine (serotonin, 5-HT) homeostasis. To examine a potential anesthetic action that could account for these observations, the effect of enflurane on 5-HT accumulation by rat brain synaptosomes was examined. Established techniques were used to prepare synaptosomes and perform uptake assays using [3H]5-hydroxytryptamine as substrate. Exposure of the synaptosomes to enflurane resulted in a concentration-dependent inhibition of serotonin uptake; the apparent I50 was 1.4 +/- 0.3 mM enflurane. Maximum inhibition was observed between enflurane concentrations of 2.6 and 4.3 mM, which inhibited uptake between 62 and 70%. The inhibition was rapid and reversible, and kinetic analysis of the inhibition was consistent with competitive inhibition by enflurane of 5-HT uptake with an apparent KI of 1.61 +/- 0.07 mM. In summary, exposure of synaptosomes to clinically relevant concentrations of enflurane resulted in a rapid, concentration-dependent, and reversible inhibition of 5-HT accumulation. These observations could represent a molecular interaction contributing to the anesthetic properties of enflurane and other volatile anesthetics.

Animals↗
PubMed1991

Volatile anesthetics and NMDA receptors. Enflurane inhibition of glutamate-stimulated [3H]MK-801 binding and reversal by glycine.

The influence of enflurane, a volatile general anesthetic, on [3H]MK-801 binding to a site in the ion channel of the N-methyl-D-aspartate (NMDA) receptor was determined in membranes from rat cerebral cortex. Enflurane disrupted glutamate stimulation of [3H]MK-801 (1 nM) binding with an IC50 of 0.4 mM. This inhibition was associated with a decrease in receptor affinity with no change in the number of [3H]MK-801 binding sites. Basal [3H]MK-801 binding measured in the absence of glutamate was not affected by enflurane. In contrast, [3H]CGS-19775 binding to the glutamate recognition site on the NMDA receptor was only weakly inhibited by enflurane (e.g., less than 20% inhibition of 5 nM [3H]CGS binding by 1.2 mM enflurane). Glycine, a positive allosteric NMDA receptor modulator, markedly attenuated the inhibition of glutamate-stimulated [3H]MK-801 binding by enflurane, with an EC50 of approximately 0.8 microM. Thus, enflurane selectively inhibits glutamate activation of the NMDA receptors, and an allosteric modulator attenuates this action. These effects could reflect anesthetic action at the glycine binding site or at another, undefined site which influences activation of the ion channel. These findings raise the possibility that inhibition of transmission at NMDA receptors contributes to the development of the anesthetic state.

Animals↗
PubMed1994

Effects of nicardipine, nitroglycerin, and nitroprusside on left ventricular diastolic function during enflurane anesthesia.

The purpose of this study was to evaluate the effects of nicardipine (NCR), nitroglycerin (NTG), or nitroprusside (SNP) on left ventricular diastolic function during enflurane anesthesia in acutely instrumented dogs. Using echocardiography, time constants for the decline in isovolumic left ventricular pressure (T), stiffness constant (K), diastolic time intervals, and left ventricular filling rates were measured in 21 mongrel dogs during the following conditions: (1) 0% enflurane (control), (2) 3.3% enflurane, (3) intravenous infusion of NCR, 1 microgram/kg/min, NTG, 2 micrograms/kg/min, or SNP, 2 micrograms/kg/min, during 3.3% enflurane, and (4) intravenous infusion of NCR, 2 micrograms/kg/min, NTG, 4 micrograms/kg/min, or SNP, 4 micrograms/kg/min, during 3.3% enflurane. During 3.3% enflurane anesthesia, T and K increased significantly, and left ventricular filling rates decreased. The administration of NCR, NTG, or SNP returned T and K to control levels. Left ventricular rapid filling rate returned toward the control level only with NCR (P < 0.05, NCR v NTG, SNP). It is concluded that the depression of diastolic function during enflurane anesthesia was improved by NCR or other vasodilators. The extent and mechanism of action of these vasodilators might differ, however.

Anesthesia, Inhalation↗
PubMed1986

[Low-concentration enflurane:study of anesthetic stability and quality of recovery].

The stability of anaesthesia and the quality of recovery obtained with low doses of enflurane were studied. Two groups of 20 patients operated for lumbar slipped disc were compared. The mean age and weight distribution of the two groups were not statistically different. Induction was the same in the two groups (diazepam, fentanyl, pancuronium and nitrous oxide). In one group, enflurane (0.4%) was added with controlled ventilation. Thiopentone was added if some spontaneous movements were observed, if arterial pressure and heart rate increased, and if the digital plethysmograph curve decreased. The quality of recovery was assessed by number-connection tests 1 and 2 h after the end of anaesthesia. Thiopentone was required five times in the group without enflurane, whilst it was never used in the group with enflurane. This difference was statistically significant (p less than 0.01) and showed a more important stability of anaesthesia when enflurane (0.4%) was used. No statistically significant difference was found in the recovery scores between the two groups 1 and 2 h after the end of anaesthesia. It was proposed that low doses of enflurane were sufficient to increase the effects of the other anaesthetic drugs without any residual effect on recovery. Low doses of enflurane could be used during anaesthesia induced with fentanyl and diazepam, giving better stability during anaesthesia without any pernicious effects on recovery.

Adult↗
PubMed1989

Enflurane-induced burst discharge of hippocampal CA1 neurones is blocked by the NMDA receptor antagonist APV.

The basis for the hyperexcitability and seizure activity associated with enflurane anaesthesia was investigated using extracellular and intracellular recording in rat hippocampal brain slices. Enflurane produced seizure-like burst discharges in CA1 pyramidal neurones, accompanied by depressed field potential amplitudes and a reduced threshold for synaptically evoked population spikes. However, threshold for action potentials evoked by intracellular current injection did not change, nor did action potential amplitude, duration or spike frequency accommodation in single neurones. Enflurane 2.0 vol% hyperpolarized CA1 neurones (3.1 (SD 1.3)mV), decreased membrane conductance (12 (6)% below control), and depressed EPSP amplitudes (34% of control) (P less than 0.01). Enflurane appeared to enhance both intrinsic and synaptically mediated inhibitory potentials. The N-methyl-D-aspartate (NMDA) receptor antagonist amino-phosphonovalerate (APV) 5-20 mumol litre-1 completely blocked seizure-like burst discharge of CA1 neurones in the presence of enflurane, and the enflurane-induced reduction of population spike threshold; it did not alter anaesthetic depression of EPSP amplitude. Thus enflurane-induced burst discharge of CA1 neurones appeared to involve an enhancement of excitatory synaptic transmission rather than depression of intrinsic or synaptic inhibition.

2-Amino-5-phosphonovalerate↗
PubMed2006

Effects of isoflurane and enflurane on GABAA and glycine receptors contribute equally to depressant actions on spinal ventral horn neurones in rats.

BACKGROUND: Volatile anaesthetics are widely used agents in clinical anaesthesia, although their mechanism of action is poorly understood. In particular, the dominant molecular mechanisms by which volatile anaesthetics depress spinal neurones and thereby mediate spinal effects such as immobility have recently become a matter of dispute. As GABAA and glycine receptors are potential candidates we investigated the impact of both receptor systems in mediating the depressant effects of isoflurane and enflurane on spinal neurones in rats. METHODS: The effects of isoflurane and enflurane on spontaneous action potential firing were investigated by extracellular voltage recordings from ventral horn interneurones in cultured spinal cord tissue slices obtained from embryonic rats (E 14-15). RESULTS: Isoflurane and enflurane reduced spontaneous action potential firing. Concentrations causing half-maximal effects (isoflurane: 0.17 mM; enflurane: 0.50 mM) were less than EC50-immobility (isoflurane: 0.32 mM; enflurane: 0.62 mM). Effects of isoflurane were mediated by 39% by glycine receptors and 36% by GABAA receptors. The effects of enflurane were mediated 26% by GABAA receptors and 29% by glycine receptors. CONCLUSION: These results demonstrate that the effects of isoflurane and enflurane on GABAA and glycine receptors contribute almost equally to their depressant actions on spinal ventral horn neurones in rats. The fraction of inhibition mediated by both receptor systems differs between specific volatile anaesthetics. Our data argue against the theory that a dominant molecular mechanism accounts for spinal effects of volatile anaesthetics.

Action Potentials↗
PubMed1997

Biotransformation of halothane, enflurane, isoflurane, and desflurane to trifluoroacetylated liver proteins: association between protein acylation and hepatic injury.

In susceptible patients, halothane, enflurane, isoflurane, and desflurane can produce severe hepatic injury by an immune response directed against reactive anesthetic metabolites covalently bound to hepatic proteins. The incidence of hepatotoxicity appears to directly correlate with anesthetic metabolism catalyzed by cytochrome P450 2E1 to trifluoroacetylated hepatic proteins. In the present study, we examined whether the extent of acylation of hepatic proteins in rats by halothane, enflurane, isoflurane, and desflurane correlated with reported relative rates of metabolism. After pretreatment with the P450 2E1 inducer isoniazid, five groups of 10 rats breathed 1.25 minimum alveolar anesthetic concentration (MAC) of halothane, enflurane, isoflurane, or desflurane in oxygen, or oxygen alone, each for 8 h. Immunochemical analysis of livers harvested 18 h after anesthetic exposure showed tissue acylation (greatest to least) after exposure to halothane, enflurane, or isoflurane. Reactivity was not different between isoflurane as compared to desflurane or oxygen alone. An enzyme-linked immunosorbent assay showed halothane reactivity was significantly greater than that of enflurane, isoflurane, desflurane, or oxygen, and that enflurane reactivity was significantly greater than desflurane or oxygen. Sera from patients with a clinical diagnosis of halothane hepatitis showed antibody reactivity against hepatic proteins from rats exposed to halothane or enflurane. No reactivity was detected in rats exposed to isoflurane, desflurane, or oxygen alone. These results indicate that production of acylated proteins may be an important mediator of anesthetic-induced hepatotoxicity.

Acylation↗
PubMed1982

Decreasing enflurane concentrations and d-tubocurarine neuromuscular blockade.

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

Adult↗
PubMed1982

The anesthetic potency of fentanyl in terms of its reduction of enflurane MAC.

Infusion rates for fentanyl were calculated to produce stable plasma concentrations at which the ability of fentanyl to reduce enflurane MAC could be studied utilizing the tail clamp method and measurement of end-tidal enflurane. Following the determination of control enflurane MAC in each animal, an infusion of fentanyl was begun. Group 1 received continuous successive infusion rates of 0.05, 0.1, and 0.2 micrograms . kg-1 . min-1 with respective loading doses (given over 20 min) of 15, 15, and 30 micrograms/kg; Group 2 received infusions of 0.2, 0.8, and 3.2 micrograms . kg-1 . min-1 with loading doses of 30, 90, and 270 micrograms/kg, respectively. Group 3 was studied in the same manner except that fentanyl was omitted from the infusion solution. Enflurane MAC was determined at each infusion level and blood samples were analyzed for the concentration of fentanyl. Fentanyl concentrations in plasma were proportional to the infusion rate. Enflurane MAC was decreased significantly in proportion to fentanyl plasma concentrations up to 30 ng/ml where a reduction of MAC by 65% was evident. A threefold higher concentration produced a minimal further reduction. In Group 3 dogs, no change in enflurane MAC was seen. It was concluded that predictable, stable levels of fentanyl in plasma can be achieved, that there is a close relationship between the concentration of fentanyl in plasma and its enflurane sparing effect, and that there is a ceiling to this concentration-response relationship.

Anesthesia, General↗
PubMed1983

Importance of myocardial loading conditions in determining the effects of enflurane on left ventricular function in the intact and isolated canine heart.

The effect of enflurane (2% and 4% inspired) on left ventricular (LV) function were examined in chronically instrumented dogs, both intact and after isolation of their hearts and lungs from the systemic circulation. Enflurane in the intact dogs increased heart rate (32 +/- 5% with 2% and 41 +/- 4% with 4%) and elicited striking, dose-dependent decreases in LV stroke shortening (-30 +/- 3% and -41 +/- 4%), the maximum velocity of LV fiber shortening, dD/dt, (-23 +/- 2%) and -40 +/- 2%), LV systolic pressure (-25 +/- 3% and -33 +/- 2%), the maximum rise of LV-pressure, dP/dt (-33 +/- 5% and -55 +/- 3%), and mean aortic pressure (-27 +/- 2% and -37 +/- 1%). However, the LV diastolic performance was impaired little, i.e., even with the higher concentration the LV end-diastolic pressure rose only moderately (32 +/- 4%), while the LV end-diastolic dimensions failed to change significantly; both LV end-diastolic pressure and LV end-diastolic diameter were decreased with the low concentration. Enflurane, after beta-adrenergic blockade alone or after combined beta-adrenergic and cholinergic blockades, or with spontaneous ventilation instead of controlled ventilation, had similar effects. By contrast, in the hearts that were isolated from the systemic circulation and the complex neurohumoral environment, enflurane increased both LV end-diastolic pressure (116 +/- 32% and 492 +/- 58%) and LV end-diastolic diameter (13 +/- 3% and 28 +/- 7%). In intact dogs with aortic pressure artificially increased to conscious control levels, enflurane likewise caused a distinct depression of the LV diastolic performance. Thus, LV systolic unloading appears to be mandatory in order to prevent acute myocardial failure from higher doses of enflurane. The observed changes in LV function with enflurane are largely independent of cardiac rate, adrenergic and cholinergic influences, and the hemodynamic consequences of intermittent positive-pressure ventilation.

Animals↗
PubMed1983

Halothane inhibits metabolism of enflurane in Fischer 344 rats.

The authors investigated the effect of prior administration of halothane upon the metabolism of enflurane. Twenty-four, one-year-old male, Fischer 344 rats were assigned randomly to four anesthetic exposure groups. Groups 1 and 2 were controls exposed only to halothane and enflurane, respectively. Group 3 was exposed for 1 h to 0.3% halothane, followed by 2 h of 1% enflurane. Group 4 was exposed for 1 h to 1% halothane and then to 2 h of 1% enflurane. Blood samples were taken prior to, immediately following, and 1, 24, and 48 h after anesthetic exposure. Serum was assayed for inorganic fluoride (F-), SGOT and SGPT. Twenty-four-hour urinary collections were assayed for F excretion. Group 1 rats exposed to halothane alone had the lowest peak mean serum F- (5.0 microM). Group 2 rats exposed to enflurane alone had the highest serum F concentration 4 h after anesthesia (18.7 microM). Peak serum F in Group 3 rats (9.5 microM) was significantly lower than in Group 2 rats (enflurane control). In Group 4 rats, serum F- was not significantly different from Group 1 rats (halothane control) at any time. In the first 24 h after anesthetic exposure, urinary F- excretion in Groups 2 and 3 was significantly higher than in Groups 1 and 4. This study demonstrated that prior exposure to halothane reduced the metabolism of enflurane; previous work suggested that this was due to an interaction of halothane with hepatic cytochrome P-450.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Effects of enflurane, isoflurane, and nitrous oxide on somatosensory evoked potentials during fentanyl anesthesia.

The effects of nitrous oxide, enflurane, and isoflurane on cortical somatosensory evoked potentials (SEPs) were studied in 29 patients undergoing intracranial or spinal operations. Anesthesia was induced with fentanyl (25 micrograms/kg, iv) plus thiopental (0.5-1.0 mg/kg, iv). In one group of patients (n = 12), nitrous oxide (50%) was compared with enflurane (0.25-1.0%), and in another group (n = 12) nitrous oxide (50%) was compared with isoflurane (0.25-1.0%). In a third group of patients (n = 5) with preexisting neurologic deficits, nitrous oxide (50%) was compared with enflurane (0.25-1.0%). In all three groups, one gas was administered for 30 min, and then the alternate gas was administered for 30 min; then the cycle was repeated for a total of two administrations of each of the two anesthetics. SEPs were determined before and after induction of anesthesia and at the end of each 30-min study period. The latencies and amplitudes of the early cortical components of the upper- and lower-extremity SEP were examined. Induction of anesthesia resulted in increases of latency in both upper- and lower-extremity SEPs without any alteration of amplitude. Nitrous oxide, enflurane, and isoflurane each decreased the amplitude of the upper-extremity SEPs compared with the postinduction value. The amplitude of the upper-extremity SEPs was less during nitrous oxide than with either enflurane or isoflurane. Nitrous oxide decreased the amplitude of lower-extremity SEPs below postinduction value, while enflurane and isoflurane had no effect. Isoflurane and enflurane increased the latency of both upper- and lower-extremity SEPs slightly, while nitrous oxide had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1988

Enflurane metabolism produces covalently bound liver adducts recognized by antibodies from patients with halothane hepatitis.

The existence of a rare syndrome of "enflurane hepatitis" similar to that described for halothane and of a cross-sensitization between halothane and enflurane has been controversial, largely due to equivocal clinical case reports and a lack of a plausible molecular mechanism for the hepatotoxicity. The present study suggests a possible hypersensitivity basis for enflurane hepatitis and the apparent cross-sensitization between halothane and enflurane involving covalently bound liver microsomal adducts. Immunoblotting studies have revealed that antibodies in the sera of six patients with halothane hepatitis recognize liver microsomal antigens of Mr = 100,000, or both 100,000 and 76,000, formed in rats treated with enflurane or halothane. These antigens were not detected in microsomes from isoflurane- or sesame oil-treated rats. The recognition of these antigens could be abolished by preincubation of the sera with microsomes from halothane-treated rats. These data suggest that the difluoromethoxydifluoroacetyl halide metabolite of enflurane, as well as the trifluoroacetyl halide metabolite of halothane, covalently bind to similar hepatic proteins, and may become immunogens in susceptible patients. This mechanism may also account for the apparent cross-sensitization between halothane and enflurane anesthesia, and the development of hepatic necrosis.

Animals↗
PubMed1993

Effects of nifedipine with isoflurane, halothane, or enflurane on automaticity, conduction, and contractility in isolated guinea pig hearts.

BACKGROUND: Calcium channel blockers and volatile anesthetics have depressant effects on cardiac function. Both groups of drugs appear to exert both qualitatively and quantitatively different effects on electrophysiologic and mechanical function. The aim of this study was to compare the direct cardiac effects of the calcium channel blocker nifedipine in the absence and presence of isoflurane, halothane, or enflurane. METHODS: Guinea pig hearts (N = 36) were isolated and perfused with oxygenated Krebs-Ringer solution (pH 7.4, 37 degrees C). Recording electrodes were placed in the right atrium and ventricle to measure heart rate and atrioventricular (AV) conduction time. Isovolumetric left ventricular pressure (LVP) was measured via a latex balloon and transducer. Hearts were randomly assigned to one of three anesthetic groups at 0.7 and 1.4 minimum alveolar concentration (MAC) and treated with 15 and 30 nM nifedipine. RESULTS: Nifedipine alone significantly decreased atrial rate and left ventricular pressure, without prolonging AV conduction. Nifedipine plus isoflurane, halothane, or enflurane did not significantly prolong AV conduction compared with the respective anesthetic agent alone, but nifedipine plus isoflurane, halothane, or enflurane significantly decreased atrial rate compared with the effect of the anesthetic alone. Halothane or enflurane plus nifedipine significantly decreased atrial rate more than nifedipine alone or isoflurane plus nifedipine. Isoflurane, halothane, or enflurane plus nifedipine significantly depressed LVP more than the respective anesthetic agent alone. Halothane or enflurane plus nifedipine also significantly depressed LVP more than isoflurane plus nifedipine or nifedipine alone. CONCLUSIONS: This study demonstrates that the combined treatment of nifedipine and volatile anesthetics, especially enflurane, additively depresses atrial rate and contractility, but not AV conduction in vitro. In comparison with results reported previously, these effects appear less pronounced than those of the combination of volatile agents with diltiazem and, especially, verapamil.

Animals↗
PubMed1993

Anesthetics and automaticity of dominant and latent pacemakers in chronically instrumented dogs. II. Effects of enflurane and isoflurane during exposure to epinephrine with and without muscarinic blockade.

BACKGROUND: Atrial dysrhythmias precede ventricular dysrhythmias during epinephrine-anesthetic sensitization, and may be caused by an altered relationship between automaticity of primary and subsidiary pacemakers. The following hypotheses were tested: (1) epinephrine-induced pacemaker shifts with enflurane or isoflurane require intact vagal reflexes and (2) these anesthetics sensitize the atrial myocardium to epinephrine-induced dysrhythmias. METHODS: Eight dogs were instrumented for chronic electrophysiologic investigation, including electrodes at the SA node, atrial appendages, right ventricle, and His bundle, and along the sulcus terminalis. After conscious-state testing, dogs were anesthetized with isoflurane or enflurane and exposed to epinephrine, with or without atropine methylnitrate. Eight-channel ECG recordings were analyzed before and during epinephrine infusions. Atrial pacemakers were assigned values 1-6 with increasing distance from the SA node, normalized and expressed as the site of earliest activation value (SEA). RESULTS: Epinephrine increased SEA values during enflurane or isoflurane anesthesia. Atropine enhanced this increase during enflurane anesthesia, but abolished the increase during isoflurane anesthesia. Enflurane increased SEA values only when combined with atropine. Isoflurane did not increase SEA values under any test conditions. CONCLUSIONS: With enflurane, epinephrine-induced atrial pacemaker shifts in chronically instrumented dogs are caused by direct depression of SA node automaticity or a relative increase of automaticity in subsidiary atrial pacemakers. With isoflurane, pacemaker shifts are caused by reflex-induced vagal suppression of SA node automaticity and escape of latent pacemakers. Enflurane sensitizes the atrial myocardium to dysrhythmias when combined with muscarinic blockade; isoflurane does not sensitize the atrium.

Anesthesia↗
PubMed1996

Minimum alveolar concentration of halothane and enflurane are decreased in early pregnancy.

BACKGROUND: Minimum alveolar concentration (MAC) of isoflurane is decreased in early pregnancy but it is not known whether this occurs to the same extent with other inhalational anesthetics. The MAC of halothane and enflurane were compared in pregnant women undergoing elective termination of pregnancy and in nonpregnant women. METHODS: We studied 16 pregnant women scheduled for termination of pregnancy at 8 to 13 weeks gestation and 16 non-pregnant patients undergoing laparoscopic sterilization. Eight patients in each group received halothane and the others received enflurane. After inhalational induction of anesthesia and tracheal intubation, MAC was determined in each patient by observing the motor response to a 10-s, 50-Hz, 80-mA transcutaneous electric tetanic stimulus to the ulnar nerve at varying concentrations of either halothane or enflurane. The end-tidal concentration of inhalational anesthetic was kept constant for at least 15 min before each stimulus and the concentration was varied ultimately in steps of 0.05 vol% (halothane) or 0.10 vol% (enflurane) until a sequence of three alternate responses (move, not move, move) or (not move, move, not move) was obtained. Minimum alveolar concentration for each person was taken as the mean of the two concentrations just permitting and just preventing movement, and MAC for the group was the median of individual MAC values. Confidence intervals were calculated for the percentage decrease in MAC for pregnant women compared with nonpregnant women. RESULTS: The median (range) MAC of halothane, 0.58 vol% (0.53 to 0.58), and enflurane, 1.15 vol% (0.95-1.25), in the pregnant women were less than those in the nonpregnant women, 0.75 vol% (0.70 to 0.78), P = 0.0005 and 1.65 vol% (1.45 to 1.75), P = 0.0007, respectively. The percentage decrease (95% CI) in MAC for pregnant women was 27% (20 to 27%) for halothane and 30% (24 to 36%) for enflurane. CONCLUSIONS: The MAC of halothane and enflurane were reduced by a similar degree in pregnant women at 8 to 13 weeks gestation compared with nonpregnant women.

Adolescent↗