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PubMed1995

Effects of enflurane on adrenergic function in canine mesenteric artery and vein.

We examined the pre- and postsynaptic effects of enflurane on the superior mesenteric artery and vein. We measured the release of norepinephrine (NE) from sympathetic nerve terminals caused by electrical stimulation (ES) or potassium and changes in vascular smooth muscle tension. The effect of enflurane was also examined in the presence of alpha 1- and alpha 2-adrenoceptor antagonists. Enflurane (1.4 to 1.6 minimum alveolar anesthetic concentration [MAC] in the dog) did not alter basal tension, but it significantly inhibited tension development caused by 40 mM KCl and ES in the canine mesenteric artery and vein. Enflurane inhibited the KCl- and ES-induced release of NE from sympathetic nerve terminals in the canine mesenteric vein. The alpha 1- and alpha 2-adrenoceptor antagonists, corynanthine or yohimbine, did not modify the effect of enflurane on the ES-induced frequency response curve of the mesenteric artery and vein. These data suggest that enflurane has at least two sites of action in mesenteric vascular beds. One site is presynaptic where it inhibits NE release, and the other is a postsynaptic site distal to the adrenergic receptor where it inhibits the smooth muscle contraction process.

Adrenergic Fibers↗
PubMed1995

Serum fluoride concentration and urine osmolality after enflurane and sevoflurane anesthesia in male volunteers.

The purpose of this study was to measure the serum fluoride concentration after enflurane or sevoflurane anesthesia and to compare the effects of prolonged anesthesia with these drugs on renal concentrating function in male volunteers. The study was subdivided into three stages; an ascending dose study of 3.0 and 6.0 minimum alveolar anesthetic concentration (MAC) hours of sevoflurane alone, a 6.0-MAC-hour comparison of enflurane and sevoflurane, and a 9.0-MAC-hour comparison of enflurane and sevoflurane. Renal concentrating function was assessed by an 18-h period of fluid deprivation and the serum fluoride concentration was measured at intervals until 60 h postanesthesia. The maximum serum fluoride concentration was greater in the volunteers exposed to sevoflurane and reached a peak in the 9-MAC-hour sevoflurane group of 36.6 microM (SD 4.3) compared with 27.5 microM (SD 2.6) in the 9-MAC-hour enflurane group. However, the rapid decrease in the serum fluoride concentration after sevoflurane was such that there was no difference between the areas under the fluoride concentration-time curves. There were no significant differences between the median maximum urine osmolalities after enflurane or sevoflurane anesthesia. Prolonged anesthesia with enflurane or sevoflurane is not associated with impaired renal concentrating function despite an increase in the serum fluoride concentration.

Adolescent↗
PubMed2001

The minimum alveolar concentration of enflurane for laryngeal mask airway extubation in deeply anesthetized children.

UNLABELLED: The end-tidal anesthetic gas concentration required to prevent the anesthetized patient from coughing or moving during or immediately after the laryngeal mask airway (LMA) extubation is not known. We sought to determine the minimum alveolar concentration of enflurane required for the removal of the LMA in children. We studied 21 nonpremedicated children between 4 and 11 yr of age, ASA physical status I, undergoing procedures below the umbilicus. General anesthesia was induced with a mask by using sevoflurane, nitrous oxide, and oxygen, and the LMA was inserted. Anesthesia was maintained with enflurane, nitrous oxide, and oxygen. At the end of surgery, a predetermined end-tidal enflurane concentration was achieved, and the LMA was removed. Each concentration at which the LMA extubation was attempted was predetermined by the up-and-down method (with 0.1% as a step size). When LMA removal was accomplished without coughing, clenching teeth, or gross purposeful muscular movements during or within 1 min after removal, it was considered a successful LMA removal. Removal was considered to be unsuccessful in patients who developed breath holding or laryngospasm during or immediately after LMA removal. The minimum alveolar concentration of enflurane at which 50% of children had a successful LMA removal was found to be 1.02% (95% CL, 0.95%-1.11%), and the 95% effective dose for successful extubation was 1.14% (95% CL, 1.07%-1.66%). In conclusion, the LMA removal may be accomplished without coughing or moving at 1.02% end-tidal enflurane concentration in 50% of anesthetized children aged 4-11 yr. IMPLICATIONS: There may be fewer problems associated with the laryngeal mask airway extubation when patients are deeply anesthetized. The purpose of this study was to determine the minimum concentration of enflurane for successful removal of the laryngeal mask in children.

Anesthesia, Inhalation↗
PubMed1980

Respiratory waveform and rebreathing in T-piece circuits: a comparison of enflurane and halothane waveforms.

The effects of respiratory waveform on rebreathing in a modified Mapleson D circuit were studied in 18 healthy adult patients anesthetized with either enflurane or halothane. At high fresh gas flow (FGF) rate, when no rebreathing of CO2 occurred, the duration of inspiration (Ti) with enflurane was 41 per cent greater than that with halothane. With enflurane there was a characteristic long end-expiratory pause, 0.69 s, whereas with halothane it was only 0.196 s. The mean inspiratory flow rate (Vt/Ti) was higher (224 ml/s) when halothane was used than with enflurane (187 ml/s). When the FGF rate was reduced to 100 ml/kg/min in the modified Mapleson D circuit, patients breathing halothane had increases in minute volumes (VE) in response to increases of 53-75 per cent in inspired volumes of CO2. The increases in VE resulted fro increases in Vt/Ti of 34-38 per cent. The volume of CO2 inspired when enflurane was used did not increase until FGF rate was as low as 70 ml/kg/min. The reduced rebreathing was related to the respiratory waveform. The advantage of reduced rebreathing with enflurane is counter-balanced by the more profound respiratory depression it causes. The FGF needed to abolish rebreathing of CO2 is highly variable, and is dependent on respiratory waveform.

Adult↗
PubMed1981

Lidocaine and pentylenetetrazol seizure thresholds in cats are not reduced after enflurane anesthesia.

Some previous reports indicate that the excitability of the brain may be increased for days following enflurane anesthesia. The authors investigated this possibility in cats by determining whether or not pentylenetetrazol- (Metrazol) or lidocaine-seizure thresholds decreased after repeated enflurane exposure. The lidocaine-seizure threshold was bracketed in 4 cats, and the pentylenetetrazol-seizure threshold was bracketed in another 4 cats. Each cat was then exposed to 4 per cent enflurane for 2 hours on 4 successive days. Twenty-four hours after the last enflurane exposure, the cats were injected with the previously determined subthreshold dose of pentylenetetrazol (6.4 mg/kg, on the average) or lidocaine (7.8 mg/kg, on the average). No cat convulsed. It was therefore concluded that under our experimental conditions, repeated enflurane exposure does not increase the sensitivity to drugs which nonselectively excite the central nervous system (e.g., pentylenetetrazol) or to drugs which mimic temporal lobe epilepsy (e.g., lidocaine). This finding cast doubt that brain excitability is increased in the post-enflurane anesthetic period.

Anesthesia↗
PubMed1983

Effects of halothane and enflurane on right ventricular performance in hearts of dogs anesthetized with pentobarbital sodium.

The effects of enflurane and halothane on contractile force of the right ventricle were compared using the Walton-Brodie strain gage arch and pulmonary artery catheter data in dogs anesthetized with pentobarbital. Twenty mongrel dogs were studied to determine the effects of the two anesthetics on contractile force during a 30-minute exposure to four approximate multiples of MAC: 0.75, 1.0, 1.25, and 2.0, and during a 2-h exposure to 1.0 MAC of each agent. Both anesthetics caused a dose-dependent reduction in contractile force, cardiac output, and mean arterial blood pressure. Enflurane caused greater depression of all variables at all concentrations tested. After a 30-min exposure to 0.75, 1.0, 1.25, and 2.0 MAC, halothane depressed contractile force 33.9%, 37.9%, 46.1%, and 73.4%, respectively, and enflurane depressed contractile force 48.4%, 53.5%, 66.6%, and 81.3%, respectively. The depression produced by enflurane at 1.0 and 1.25 MAC was significantly greater (P less than 0.05) than the depression produced by halothane at equal MAC. The reduction of cardiac output by enflurane at 1.25 and 2.0 MAC was significantly greater than that observed with halothane (P less than 0.05). The decrease in mean blood pressure produced by enflurane was significantly greater (P less than 0.05) than the decrease produced by halothane at 1.0, 1.25, and 2.0 MAC. No significant differences between groups were found in temperature, arterial PCO2, PO2, pH, or hematocrit levels. No diminution of the differences in effect on contractility between the two agents was observed when the exposure period was lengthened to two hours at 1.0 MAC.

Anesthesia, General↗
PubMed1984

Vecuronium-induced neuromuscular blockade during enflurane, isoflurane, and halothane anesthesia in humans.

To determine the effect of the commonly used volatile anesthetics on a vecuronium-induced neuromuscular blockade, the authors studied 54 patients anesthetized with 1.2 MAC or 2.2 MAC enflurane, isoflurane, or halothane (MAC value includes contribution from 60% nitrous oxide). During 1.2 MAC enflurane, isoflurane, and halothane, the ED50S (the doses depressing twitch tension 50%) for vecuronium were 12.8, 14.7, and 16.9 micrograms/kg, respectively. During 2.2 MAC enflurane, isoflurane, and halothane, the ED50S for vecuronium were 6.3, 9.8, and 13.8 micrograms/kg, respectively (P less than 0.05). Time from injection to peak effect was the same for each anesthetic group (6.5 +/- 0.5 min, mean +/- SD), except for the group given 2.2 MAC enflurane (9.7 +/- 0.6 min) (P less than 0.05). The duration of a 50% block from injection to 90% recovery was the same for each group (mean 20 +/- 4 min), except for the group given 2.2 MAC enflurane (46.5 min) (P less than 0.05). The authors conclude that enflurane is the most potent volatile anesthetic, followed by isoflurane and then halothane, in augmenting a vecuronium-induced neuromuscular blockade. Increasing the concentration of volatile anesthetic has less effect on a neuromuscular blockade produced by vecuronium than on one produced by other nondepolarizing relaxants (e.g., pancuronium and d-tubucurarine).

Dose-Response Relationship, Drug↗
PubMed1984

Comparison of cardiovascular responses to verapamil during enflurane, isoflurane, or halothane anesthesia in the dog.

The cardiovascular responses to increasing infusion rates of the slow calcium channel inhibitor, verapamil, were studied in three groups of dogs during either enflurane, isoflurane, or halothane anesthesia. Control hemodynamic values and plasma samples were taken after 2 h of anesthesia with the given agent. Increasing infusion rates of verapamil were given to achieve a range of plasma verapamil levels up to approximately 500 ng X ml-1. Each infusion rate was administered for 30 min, at which time repeat measurements and plasma samples for verapamil were taken. Mean arterial blood pressure, cardiac index, and left ventricular dP/dt decreased with increasing plasma verapamil levels in the enflurane and isoflurane groups compared with the control values. The values for the enflurane-verapamil combination were significantly lower than those for the other anesthetics at comparable verapamil levels. Compared with enflurane, higher verapamil levels were required with isoflurane to achieve the equivalent degree of hemodynamic depression. A higher incidence of conduction abnormalities also was noted in the enflurane group. In the halothane group, the only significant change observed at these verapamil levels, achieved by continuous infusion, was a prolongation of the PR interval of the ECG. In this animal model, verapamil was least well tolerated by the cardiovascular system during enflurane anesthesia.

Anesthesia, General↗
PubMed1985

Inhibition and stimulation of enflurane metabolism in the rat following a single dose or chronic administration of ethanol.

The effects of a single oral dose or chronic ingestion of ethanol on in vivo and in vitro metabolism of enflurane were studied in Fischer 344 rats. At various intervals after ethanol treatment, enflurane was administered ip and 1 h after enflurane administration fluoride and ethanol levels were measured in plasma and hepatic microsomes were prepared. The concentration of ethanol in plasma (+/- SE) was 0.138 +/- 0.035% at 9 h after the single dose of ethanol and decreased almost to control levels by 17 h. The hepatic microsomal defluorination of enflurane was enhanced 3.5-fold and 6.3-fold at 9 and 25 h after the ethanol dose and returned to the control level by 33 h. In vivo defluorination was inhibited almost completely at 8 h after the ethanol dose, increased to 3.4 times the control level at 24 h, and decreased to the control level by 32 h. At 1 h after the end of chronic ethanol treatment, the concentration of ethanol in plasma was 0.254 +/- 0.018%, and it decreased to the control level by 9 h. Hepatic microsomal enflurane defluorinating activity was increased 10.5-fold at 1 h after the end of chronic treatment and decreased to the control level by 13 h. Immediately following chronic treatment, enflurane defluorination in vivo was almost totally inhibited. It increased to 9.3 times the control level at 4 h after chronic treatment was stopped and then decreased to nearly the control level at 12 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗
PubMed1985

Anticonvulsant actions of enflurane on epilepsy models in cats.

The effects of enflurane on three epilepsy models were studied in cats. The models used were seizures in amygdaloid kindled cats and those induced by bicuculline and penicillin. The authors found that not only a subconvulsive (1.5%) but a convulsive (3.5%) dose of enflurane suppressed the seizures in all models. There was no sign of activation by enflurane of the epileptic focal activities in the dose range studied: the penicillin-induced cortical seizure was suppressed completely, and the threshold dose of bicuculline required to induce seizure in normal cats and the threshold current required to induce seizure in amygdaloid-kindled cats were both increased by both the subconvulsive and convulsive dose of enflurane. The pattern of suppression was, however, dissimilar in each model. It was dose dependent in the case of penicillin-induced seizure, while it was biphasic in several aspects in the seizures of bicuculline-induced and amygdaloid kindled models. For the subconvulsive dose the degrees of increase in the thresholds required to induce seizure in bicuculline-induced and amygdaloid-kindled models were both greater than those for the convulsive dose of enflurane. In spite of such a definite suppression of the excitability of focus, the propagation of amygdaloid after-discharge was facilitated by the convulsive dose. The intensity of convulsion induced by suprathreshold dose of bicuculline was depressed in a dose-related manner. The intensity of the convulsion in the amygdaloid-kindled model was also suppressed when it was estimated by visual inspection of behavior and the degree of activation of the brain electrical activities. The authors conclude that there is little, if any, exacerbation by enflurane of preexisting epileptic foci, the only exception possibly being the case of certain myoclonic type epilepsies such as progressive myoclonic epilepsy and photosensitive epilepsy. This anesthetic probably can be used with a considerable degree of safety for epileptic patients.

Amygdala↗
PubMed1991

The effects of halothane, enflurane, and isoflurane on calcium current in isolated canine ventricular cells.

The effects of halothane, enflurane, and isoflurane on voltage-dependent Ca2+ channel current (ICa) were compared in canine ventricular cells by the whole-cell voltage-clamp technique. ICa was elicited in each cell by progressively depolarizing pulses, from -80 or -40 mV to more positive membrane potentials. The peak amplitude and inactivation rate of the inward current were analyzed before, during, and after the external application of equianesthetic concentrations (0.5, 1.0, and 2.0 MAC) of halothane, enflurane, or isoflurane. The concentrations of these agents in the Krebs' solution were as follows (percentage in the gas phase): halothane 0.36, 0.68, and 1.50%; isoflurane 0.50, 1.00, and 1.90%; and enflurane 0.66, 1.36, and 2.39%. Halothane, enflurane, and isoflurane rapidly reduced peak ICa amplitude at all voltages studied, resulting in a depression of the entire current-voltage relationship for ICa activation. This depression was concentration-dependent and completely reversible upon wash-out of the anesthetic agents. Quantitatively, the three anesthetic agents produced a similar inhibition of peak ICa at approximately equianesthetic concentrations. Inactivation of ICa during 200-ms depolarizing pulses was not affected by two lower concentrations of the anesthetic agents, but was accelerated by the highest concentration of enflurane used. These findings suggest that the negative inotropic and chronotropic actions of halothane, enflurane, and isoflurane on the ventricular myocardium are related, at least in part, to their inhibition of ICa at the sarcolemma. However, since all three anesthetic agents depressed ICa amplitude similarly, their quantitatively different effects on cardiac performance are due most likely to differences in actions at other cellular sites.

Animals↗
PubMed1994

Halothane and enflurane constrict canine mesenteric arteries by releasing Ca2+ from intracellular Ca2+ stores.

BACKGROUND: Recent studies suggest that volatile anesthetics cause not only vasodilation but also vasoconstriction, depending on the experimental conditions. However, the mechanism of the constrictive effect of volatile anesthetics has not been clarified. The aim of this study was to evaluate the vasoconstrictor effects of halothane, enflurane, and isoflurane and to elucidate the underlying mechanism. METHODS: Vascular rings of canine mesenteric arteries were mounted in organ baths, and isometric tension changes were recorded. Changes in intracellular free Ca2+ concentration of vascular smooth muscle were examined by using the fluorescent Ca2+ indicator fura 2 and a dual-wavelength fluorometer. RESULTS: Halothane (0.75-2.3%) and enflurane (1.7-3.4%), but not isoflurane (1.2-3.5%), induced a concentration-dependent transient contraction, followed by a slight, sustained contraction. Halothane (1.5%)- and enflurane (3.4%)-induced contractions were reduced by endothelial denudation and enhanced by indomethacin (10(-5) M) treatment but were not affected by L-NG-nitroarginine (10(-5) M) or nifedipine (2 x 10(-7) M) treatment. Ryanodine (2 x 10(-5) M) treatment completely abolished the transient increases in tension and Ca2+ concentration. Even in ryanodine-treated arteries, however, both anesthetics induced a slowly developing sustained contraction, and the sustained contraction induced by enflurane (3.4%) was not accompanied by a significant increase in Ca2+ concentration. CONCLUSIONS: Halothane and enflurane, but not isoflurane, induce vasoconstriction by releasing Ca2+ from intracellular stores. Release of a vasodilating prostanoid and endothelium-derived constricting factor may also be involved in the vasoconstrictor effect. Furthermore, increased Ca2+ sensitivity of contractile machinery may be involved in the effect of enflurane.

Animals↗
PubMed1995

Arterial oxygenation during one-lung ventilation. A comparison of enflurane and isoflurane.

BACKGROUND: Because maintaining arterial oxygenation (PaO2) during one-lung ventilation (OLV) can be a clinical problem, it is useful to be aware of factors that influence PaO2 in this situation and are under the control of the anesthesiologist. It is unknown whether, among the commonly used volatile anesthetic agents, one is associated with higher PaO2 levels. Clinical studies suggest that isoflurane provides superior PaO2 during OLV than does halothane. These have not been compared to enflurane. The authors studied PaO2 and hemodynamics during OLV with 1 MAC enflurane versus 1 MAC isoflurane. METHODS: Twenty-eight adults who had prolonged periods of OLV anesthesia with minimal trauma to the nonventilated lung (thoracoscopic or esophageal surgery) were studied in a cross-over design. Patients were randomized to two groups: Group 1 received 1 MAC enflurane in oxygen from induction until after the first 30 min of OLV, then were switched to 1 MAC isoflurane. In group 2, the order of the anesthetics was reversed. RESULTS: Isoflurane was associated with higher PaO2 values during OLV (P < 0.0001). Mean PaO2 (+/- SD) after 30 min OLV isoflurane was 231 (+/- 125) mmHg versus 184 (+/- 106) mmHg after 30 min OLV enflurane. The difference in PaO2 between the two anesthetics was most marked in the patients with the highest PaO2 during OLV: PaO2 isoflurane PaO2 enflurane varies; is directly proportional to PaO2 isoflurane (r = 0.65, P < 0.001). There were no other significant differences between anesthetic gases in the measured hemodynamic or respiratory variables. In the subgroup of patients with pulmonary artery catheters (n = 7), PaO2 correlated with cardiac output during OLV for both anesthetics (r = 0.81, P < 0.001). CONCLUSIONS: During OLV, the PaO2 values with 1 MAC isoflurane were greater than those with enflurane. The dependence of PaO2 on cardiac output does not support the hypothesis that an increase in cardiac output will cause a decrease in hypoxic pulmonary vasoconstriction and a decrease in PaO2 during OLV.

Adult↗
PubMed2001

Enflurane actions on spinal cords from mice that lack the beta3 subunit of the GABA(A) receptor.

BACKGROUND: Gamma-aminobutyric acid type A (GABA(A)) receptors are considered important in mediating anesthetic actions. Mice lacking the beta3 subunit of this receptor (beta3-/-) have a higher enflurane minimum alveolar concentration (MAC) than wild types (+/+). MAC is predominantly determined in spinal cord. METHODS: The authors measured three population-evoked responses in whole spinal cords, namely, the excitatory postsynaptic potential (pEPSP), the slow ventral root potential (sVRP), and the dorsal root potential. Synaptic and glutamate-evoked currents from motor neurons in spinal cord slices were also measured. RESULTS: Sensitivity of evoked responses to enflurane did not differ between +/+ and -/- cords. The GABA(A) receptor antagonist bicuculline significantly (P < 0.05) attenuated the depressant effects of enflurane on pEPSP, sVRP and glutamate-evoked currents in +/+ but not -/- cords. The glycine antagonist strychnine elevated the pEPSP to a significantly greater extent in -/- than in +/+ cords, but the interactions between strychnine and enflurane did not differ between -/- and +/+ cords. CONCLUSIONS: Similar enflurane sensitivity in spinal cords from -/- and +/+ mice was coupled with a decreased role for GABA(A) receptors in mediating the actions of enflurane in the former. This finding implies that other anesthetic targets substitute for GABA(A) receptors. Increase in glycine receptor-mediated inhibition was found in -/- cords, but the glycine receptor does not appear to be a substitute anesthetic target. This mutation thus led to a quantitative change in the molecular basis for anesthetic depression of spinal neurotransmission in a fashion not predicted by the mutation itself. The results argue against an immutable dominant role for GABA(A) receptors in mediating spinal contributions to MAC.

Anesthetics, Inhalation↗
PubMed2001

Characterization of thioether compounds formed from alkaline degradation products of enflurane.

BACKGROUND: Renal toxicity has occasionally been observed after enflurane anesthesia. Although originally attributed to its oxidative metabolism to inorganic fluoride, serum levels of inorganic fluoride appear to be small to explain these renal effects. Formation of potentially nephrotoxic halogenated alkenes during alkaline degradation in carbon dioxide absorbers and subsequent bioactivation via the glutathione conjugation pathway may be considered as an alternative mechanism for renal toxicity. The aim of this study was to characterize the thioethers formed chemically and biosynthetically. METHODS: Alkaline degradation of enflurane was achieved by stirring with pulverized potassium hydroxide. Volatile degradation products were analyzed by 19F nuclear magnetic resonance (NMR) analysis of head space gasses trapped in dimethyl sulfoxide (DMSO). Thioethers were generated chemically by trapping head space gasses in DMSO containing N-acetyl-L-cysteine or 2-mercaptoacetic acid as model thiol compounds. Glutathione conjugates were generated biosynthetically by passing head space through rat liver fractions in presence of glutathione. Products formed were analyzed by gas chromatography-mass spectroscopy and 19F-NMR. RESULTS: Direct analysis of head space gasses showed formation of 1-chloro-1,2-difluorovinyl difluoromethyl ether and two unidentified fluorine-containing products as alkaline degradation products of enflurane. When trapped in DMSO-N-acetyl-L-cysteine-triethylamine, N-acetyl-S-(2-chloro-1,2-difluoro-1-(difluoromethoxy)ethyl)-L-cysteine was identified as the major product. Another N-acetyl-L-cysteine S-conjugate formed was N-acetyl-S-(2-chloro-1,1,2-trifluoroethyl)-L-cysteine, a potent nephrotoxin in rats. 19F-NMR analysis of glutathione conjugates formed after incubation with rat liver fractions resulted in formation of corresponding S-conjugates. CONCLUSIONS: The current study demonstrates that alkaline degradation products of enflurane can be conjugated to thiol compounds, forming S-conjugates that could theoretically contribute to adverse renal effects observed occasionally with enflurane anesthesia. The N-acetyl-L-cysteine S-conjugates identified may be biomarkers to assess exposure of humans to alkaline degradation products of enflurane.

Acetylcysteine↗
PubMed1987

Total body oxygen supply-demand balance in burned patients under enflurane anesthesia.

The effects of enflurane anesthesia on the oxygen supply-demand balance have been studied in nine hypermetabolic-hyperdynamic burned patients undergoing debridement and skin-grafting procedures. Mean burn size was 55% of total body surface area. The patients were without cardiac, lung, hepatic, and kidney dysfunction and were not septic. Anesthesia was induced with sodium pentothal and maintained with enflurane and nitrous oxide in oxygen. Ventilation was controlled to maintain PaCO2 within normal limits. Crystalloid solutions and blood were administered to maintain adequate heart filling pressures. Serial measurements of cardiac output, arterial and mixed venous blood gases, and oxygen content were made before, during, and after anesthesia. Following induction of anesthesia and enflurane administration, cardiac output, oxygen delivery, and oxygen consumption decreased in a parallel fashion to approximately 60% of control. These variables did not change significantly throughout the procedure and returned to control values when enflurane was discontinued. Arteriovenous oxygen content difference did not increase and metabolic acidosis did not develop, suggesting that tissue perfusion remained adequate. Under anesthesia, oxygen consumption in burned patients was similar to that observed in normal subjects, indicating that enflurane blunts the hypermetabolic effects of thermal injury. It is concluded that in burned patients enflurane decreases metabolic rate and cardiac output, and maintains an adequate oxygen supply-demand balance.

Adolescent↗
PubMed1979

Comparative effects of repeated and prolonged inhalation exposure of beagle dogs and Cynomolgus monkeys to anaesthetic and subanaesthetic concentrations of enflurane and halothane.

Male and female Beagle dogs and Cynomolgus monkeys were exposed to anaesthetic (1.5 MAC) and subanaesthetic (1/100 MAC) levels of enflurane and halothane for 3 hours on alternate days for 4 weeks. One-half of the animals were killed following the last exposure and the remainder after 4 weeks of recovery. The animals' condition was assessed during anaesthetic periods by measuring respiration, ECG, blood pressure, temperature and EEG. Haematology, urinalysis and clinical chemistry parameters were evaluated. Gross and microscopic pathological examinations were conducted at the end of the exposure and recovery periods. Two female monkeys in the mid- and high-dose halothane groups died during the study. No deaths were observed in the enflurane group. No quantitative differences were observed in respiration rate, heart rate, blood pressure and EEG activity of animals anaesthetized with enflurane or halothane. Muscle twitches were observed in some mid- and high-dose dogs inhaling enflurane, but not in monkeys. A number of liver function tests became abnormal in mid- and high-dose halothane-treated dogs and high-dose halothane-treated monkeys. This was not observed with enflurane. Histopathologic alterations were confined to the liver of animals exposed to halothane. In dogs, the lesions were characterized by centrilobular hepatocyte degeneration and/or necrosis, fibroblastic proliferation, hepatocyte enlargement, fat deposition and glycogen depletion; and in mid- and high-dose monkeys by moderate to marked hepatocyte vacuolation and fat deposition. Except for one high-dose dog, these lesions were not seen in animals killed after 4 weeks of recovery. No histopathologic alterations were observed with enflurane.

Alanine Transaminase↗
PubMed1982

Effect of mannitol and furosemide on urinary fluoride excretion of surgical patients anaesthetized with enflurane or halothane.

Urinary excretion of fluoride after enflurane anaesthesia has been found to correlate with urinary pH, while the correlation with urinary volume has remained unsettled. We therefore studied the effect of moderate doses of mannitol and furosemide on serum fluoride levels and urinary excretion of fluoride in surgical patients after controlled doses of enflurane (6+6+6 patients) or halothane (5+5+5 patients). The highest serum fluoride level was 31 mumol/1 in an enflurane patient (enflurane dose 1.26 end-tidal vol % x h) and 8 mumol/1 in a halothane patient (halothane dose 0.59 end-tidal vol. % x h). Mannitol caused th greatest mean excretion of fluoride (not significant (n.s)) in the enflurane patients without any marked rise in urinary pH or volume. Furosemide increased urinary output markedly but did not enhance urinary fluoride excretion or raise urinary pH. Compared with the control groups of both inhalation anaesthetic patients, the diuretics appeared to have no effect on the serum fluoride levels. In the enflurane patients there was a positive correlation between the change in fluoride clearance and the change in urinary pH, but no with the change in urinary volume during the first postoperative hours. On the other hand, in the halothane patients there was a positive correlation between the change in fluoride clearance and the change in urinary volume. A possible "fluoro-uretic" action of mannitol was also seen in the halothane patients, as in the later postoperative period fluoride excretion was greatest when mannitol had been given.

Adult↗