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PubMed1984

Effect of enflurane, isoflurane, and nitrous oxide on the microbicidal activity of human polymorphonuclear leukocytes.

The effect of enflurane and isoflurane with and without nitrous oxide (N2O) on human polymorphonuclear leukocyte (PMNL) microbicidal function was studied. Bacterial killing was determined using a standard pour-plate technique and by oxidative activity as measured by chemiluminescence (CL). No killing of Escherichia coli, Klebsiella pneumoniae, or Staphylococcus aureus was seen at bacteria:PMNL ratios of 1 or 10:1 with either enflurane or isoflurane at concentrations greater than normally used (3%). However, at a clinically relevant concentration of 2%, a significant inhibition of bacterial killing was observed with enflurane but not isoflurane at a bacteria:PMNL ratio of 100:1. The CL response also was decreased significantly (28% inhibition) by 2% enflurane. N2O 70% plus O2 30% had no effect on bactericidal activity or chemiluminescence alone or in combination with enflurane or isoflurane. The inhibition of bacterial killing and CL following enflurane exposure could be reversed by exposing the enflurane treated PMNL to air for 30 min. These results suggest that enflurane is able to inhibit PMNL microbicidal activity only when the PMNL are stressed with a large bacterial challenge or stimulus. This inhibition is temporal and only occurs during enflurane exposure.

Blood Bactericidal Activity↗
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↗
PubMed1993

Inhibition by enflurane of baroreflex mediated mesenteric venoconstriction in the rabbit ileum.

BACKGROUND: Halothane and isoflurane are known to attenuate neurally mediated regulation of mesenteric vein diameter. The current study evaluated the effects of enflurane on baroreflex control of small mesenteric veins. METHODS: Changes in mesenteric vein diameter, intravenous pressure, mean arterial pressure, and heart rate in response to bilateral carotid occlusion, aortic nerve stimulation, and celiac ganglion stimulation were measured in 23 chloralose-anesthetized rabbits before, during, and after 1% and 2% inhaled enflurane administration. In six other rabbits, sympathetic efferent nerve activity was recorded directly from a postganglionic splanchnic nerve, also during bilateral carotid occlusion and aortic nerve stimulation, before, during, and after inhalation of 1% and 2% enflurane. RESULTS: Baseline mean arterial pressure and heart rate decreased, and mesenteric vein diameter increased, in response to inhaled enflurane. Reflex venoconstriction and the increases in mean arterial pressure, intravenous pressure, and heart rate, in response to bilateral carotid occlusion, were significantly inhibited at both levels of inhaled enflurane. Decreases in mean arterial pressure and heart rate, and reflex venodilation in response to aortic nerve stimulation, were attenuated by 2%, but not 1%, enflurane. Mesenteric venoconstriction, blood pressure increase, and bradycardia in response to celiac ganglion stimulation were unaffected by 2% inhaled and 5% superfused enflurane. Both 1% and 2% inhaled enflurane attenuated resting and carotid sinus-mediated increases in sympathetic efferent nerve activity. CONCLUSIONS: These results indicate that enflurane alters splanchnic venous reflexes in large part via the inhibition of sympathetic efferent activity.

Administration, Inhalation↗
PubMed1993

Effects of isoflurane and enflurane on intracellular Ca2+ mobilization in isolated cardiac myocytes.

BACKGROUND: Enflurane and isoflurane may reduce cardiac contractility by altering mobilization and clearance of intracellular Ca2+ (Ca2+i). It was hypothesized that the negative inotropic actions of these agents involve limiting both membrane Ca2+ entry and altering intracellular Ca2+ release. METHODS: The Ca2+i transients in rat ventricular myocytes loaded with fura-2 were recorded from a fluorescence microscope. Transients stimulated by membrane depolarization (suction electrode or elevated [K+]o) or 15 mM caffeine to release Ca2+ from the sarcoplasmic reticulum (SR) were analyzed for net amplitude, maximal rate of rise (VR), average rate of decline (VR) in [Ca2+]i, and duration. RESULTS: Enflurane and isoflurane reduced electrically stimulated Ca2+i transients in a dose-dependent manner. Enflurane depressed the Ca2+i transient amplitude more than isoflurane. Enflurane was more effective than isoflurane in reducing VR and VF in a concentration-dependent manner. At similar concentrations, both enflurane and isoflurane reduced the steady state elevation of [Ca2+]i by 50 mM K+o. Similarly, enflurane and isoflurane depressed caffeine-sensitive release of Ca2+ from the SR. The reduction in the Ca2+i transient because of SR Ca2+ release was greater in enflurane than in equal concentrations of isoflurane. Rates of elevation and decline in [Ca2+]i were also reduced in enflurane and isoflurane. CONCLUSIONS: The negative inotropic actions of enflurane and isoflurane involve a depression of Ca2+ influx during membrane excitation, as well as a reduction in SR Ca2+ release. Slowed rates of elevation in [Ca2+]i indicate that the latter mechanism may, in part, be caused by alterations in the kinetics of SR Ca2+ release.

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↗
PubMed1990

Enflurane depresses activity of the medullary inspiratory neurons in the cat.

The effect of enflurane on the firing activity (spikes/sec) of the inspiratory neurons of the dorsal respiratory group (DRG) of the medulla oblongata was studied in decerebrate, paralyzed, mechanically ventilated cats before and after bilateral cervical vagotomy. Inspiratory neuronal activity, phrenic neurogram, arterial blood pressure, tracheal pressure, and end tidal CO2 concentration were recorded. Cells whose firing activity was in phase with that of the phrenic nerve were considered inspiratory neurons. Administration of 1 and 2% enflurane in oxygen produced gradual, significant, and dose-dependent depression of the cell activity with cervical vagi either intact or severed. Recovery of the cell activity occurred after termination of enflurane administration. In cats with intact vagi, 10 min after introduction of 1 and 2% enflurane, the cell activity (mean +/- SE) expressed as percentage of the control was 70 +/- 6% (P less than 0.05) and 48 +/- 5% (P less than 0.01), respectively. Bilateral cervical vagotomy did not affect the degree of cell depression due to enflurane. Hypercarbia induced by inhalation of 5% CO2 increased cell activity, but it did not block enflurane-induced cell depression, although it reduced it. It may be concluded that enflurane depresses the activity of the inspiratory neurons of the DRG. The results also suggest that the respiratory depressant effect of enflurane has a central component and that the DRG region may serve as a site to mediate the enflurane-induced respiratory depression.

Animals↗
PubMed1992

[Amrinone reverses cardiac depression by enflurane in the dog].

To evaluate the interaction of amrinone with inhalational anesthetics, cardiovascular effects of amrinone were investigated in nine mongrel dogs anesthetized with enflurane. Each dog received enflurane and amrinone in the following sequence: 1) 2% enflurane alone, 2) continuous infusion of 20 micrograms.kg-1.min-1 during enflurane, 3) 40 micrograms.kg-1.min-1 infusion during enflurane. Amrinone 40 micrograms.kg-1.min-1 during enflurane anesthesia improved the maximum left ventricular dP/dt, stroke volume and decreased effective arterial elastance (Ea) without changes in left ventricular end-diastolic pressure and heart rate. Left ventricular pressure (LVP) and systolic femoral arterial pressure were stable, but diastolic femoral arterial pressure decreased significantly from enflurane anesthesia alone. These parameters at 20 micrograms.kg-1.min-1 of amrinone infusion during enflurane showed the same tendency with 40 micrograms.kg-1.min-1 infusion but not significantly different from enflurane alone. This result suggests that amrinone may be beneficial in the patients with depression of cardiac performance during anesthesia.

Amrinone↗
PubMed1989

Left ventricular oxygen tensions in dogs during coronary vasodilation by enflurane, isoflurane and dipyridamole.

The purpose of this study was to investigate the effects of the anesthetics enflurane and isoflurane and of the coronary vasodilator dipyridamole on myocardial oxygen balance and myocardial tissue oxygen tensions. The studies were performed in 24 open-chest dogs during basal anesthesia with a narcotic. Myocardial blood flow (MBF) was measured using radioactive microspheres, myocardial surface tissue PO2 by means of a platinum multiwire surface electrode. One control group and three experimental groups were studied: enflurane (1.1 vol%), isoflurane (0.7 vol%, both end-tidal concentrations), and dipyridamole (0.4 mg/kg). Mean arterial pressure significantly decreased to an average of 70 mm Hg in all three experimental groups. Although MBF was unchanged during enflurane (-18%) and isoflurane (+20%), it increased during dipyridamole (+304% p less than 0.05 vs baseline and control, enflurane, and isoflurane groups). Myocardial oxygen consumption decreased significantly during enflurane and isoflurane but remained unchanged during dipyridamole. Thus, the ratio between myocardial oxygen delivery and consumption increased 6% with enflurane (p less than 0.05 vs baseline), 47% with isoflurane (p less than 0.05 vs baseline and control group) and 280% with dipyridamole (p less than 0.05 vs baseline and control, enflurane, and isoflurane groups). Coronary venous PO2 remained unchanged during enflurane but increased significantly during isoflurane and dipyridamole. Left ventricular surface tissue PO2 was unchanged in enflurane and isoflurane animals and decreased slightly, yet significantly, during dipyridamole. All variables remained unchanged in the control group. Thus, isoflurane and dipyridamole interfered with MBF autoregulation and increased myocardial oxygen delivery out of proportion to myocardial demands.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Effects of enflurane on release of insulin by pancreatic islets in vitro.

The effects of enflurane upon rate of insulin release from rat pancreatic islets were determined in vitro. A dose-related inhibitory effect of enflurane on glucose-stimulated insulin release was observed with almost complete inhibition being seen when the enflurane concentration in the gas phase was 3.21% (v/v), equivalent to 1.26 mM enflurane in the liquid phase. The onset on enflurane-induced inhibition was rapid, being fully developed within 5 minutes of islet exposure to the agent while the effect was equally rapidly reversed on removal of enflurane from the medium. As glucose metabolism is known to be required for glucose-stimulated insulin secretion to occur, rates of islet metabolism of [U-14C] glucose to 14CO2 were examined but these were unaffected by concentrations of enflurane up to 2.21 mM. To investigate further the metabolic integrity of islets, rates of islet incorporation of L-[4,5-3H] leucine were determined; these too were not significantly altered by concentrations of enflurane up to 1.26 mM. It is concluded that enflurane in the concentration range used clinically leads to a rapid, reversible inhibition of rat pancreatic islet insulin release, which is not attributable to interference with islet glucose metabolism or protein biosynthesis.

Animals↗
PubMed1980

Disposition of enflurane in obese patients.

The disposition of enflurane, a volatile halogenated anesthetic, was studied in obese (n = 26) and nonobese (n = 8) consenting adult subjects undergoing elective intra-abdominal surgical procedures. Enflurane and fluoride ion, a nephrotoxic metabolite of enflurane, were measured in the blood of subjects before, during and up to 24 hr after exposure to pharmacologically equivalent doses of enflurane [approximately 2.0 MAC hr (the minimal alveolar concentration at which 50% of humans do not respond to a painful stimulus)] Arterial enflurane in obese subjects reached maximal concentrations 3 times faster than nonobese subjects who reached similar blood levels 80 min after the initiation of anesthesia. The blood/gas partition coefficient for enflurane in the obese was found to be 30% lower than that in the nonobese (0.99 +/- 0.02 vs. 1.42 +/- 0.02) and may possibly explain the observed differences in enflurane uptake. The rate at which inorganic fluoride appeared in obese serum (5.5 microM/hr) was twice that seen in the nonobese group. No differences in urinary fluoride excretion were demonstrated. Maximum serum fluoride concentration occurred 2 hr postenflurane anesthesia in both groups with the obese having a 60% higher concentration (27.8 +/- 2.0 vs. 17.0 +/- 3.0 microM), indicating increased biotransformation in the obese. Hepatic triglyceride content was demonstrated to be unrelated to the increased enflurane biotransformation observed in obese subjects. Equations are presented for the estimation of mean maximum serum inorganic fluoride levels in both obese and nonobese subjects after enflurane anesthesia.

Biotransformation↗
PubMed1993

[Effect of enflurane on human somatosensory evoked potentials: differences between specific and nonspecific responses].

The effect of enflurane on somatosensory evoked potentials (SEP) was investigated in nine gynecological patients under nitrous oxide-enflurane anesthesia. SEPs were obtained from electrodes placed on the scalp C4 and earlobes by median nerve stimulation contralateral to the recording site. SEPs taken in a control study without enflurane consisted of six components; P12, N17, P23, N31, P50, and N65. Components N17, P23, N31, and P50, thought to be specific SEP responses, showed a dose-dependent increase in latencies under enflurane while P12, the initial SEP components, did not show any significant changes throughout the experiment. The longer the latency for a given response component, the greater was the increase in latency seen under enflurane anesthesia. On the other hand, N65, assumed to be a nonspecific SEP response, was completely lost with inhalation of 0.5 MAC or more of enflurane. However, the peak-to-peak amplitude between P23 and N31 was enhanced dose-dependently with enflurane up to 1.5 MAC. These results suggest that, at clinically effective doses, enflurane may inhibit nonspecific projection pathways while enhancing the primary cortical sensory area, and this enhancement may be responsible for provoking convulsive seizures under enflurane anesthesia.

Adult↗
PubMed1996

[Serum fluoride concentrations and exocrine kidney function with sevoflurane and enflurane. An open, randomized, comparative phase III study of patients with healthy kidneys].

UNLABELLED: Sevoflurane is a "new" volatile inhaled anaesthetic. Owing to its lower blood-gas solubility coefficient, emergence from anaesthesia is faster with sevoflurane than with isoflurane, enflurane, or halothane. Sevoflurane undergoes metabolic biodegradation, releasing inorganic fluoride ions that could produce nephrotoxicity. In this study, we compared serum inorganic fluoride concentrations (IFCs) in patients receiving either sevoflurane or enflurane. Furthermore, indices of renal function were evaluated until the 3rd postoperative day. METHODS: Thirty patients with no history of renal or hepatic disease and with an anticipated duration of anaesthesia of at least 3 h were studied in an open, prospective, randomised clinical trial. Anaesthesia was induced with fentanyl, thiopentone, and vecuronium for facilitating endotracheal intubation. Anaesthesia was maintained with sevoflurane or enflurane, 60% nitrous oxide in oxygen, and additional doses of fentanyl. Blood samples for serum IFCs were obtained preoperatively and 2 and, if possible, 4 and 6 h after starting sevoflurane or enflurane, at the end of anaesthesia, and 1, 2, 4, 8, 12, 24, 48 and 72 h post-anaesthesia. Fluoride analysis was performed using an ion-selective electrode. Indices of renal function (serum sodium, osmolality, creatinine, urea, and uric acid, urine specific gravity, osmolality, and pH) were evaluated preoperatively, at the end of anaesthesia, and 24, 48, and 72 h post-anaesthesia. RESULTS: The duration of anaesthetic exposure was approximately 1.65 MAC-h for both inhaled anaesthetics. Peak serum IFCs were higher with sevoflurane (34.5 mumol/l) than with enflurane (19.4 mumol/l). Fluoride levels decreased more rapidly with sevoflurane: 24 h post-anaesthesia there was no difference between sevoflurane and enflurane (Fig. 1). The area under the curve (AUC) was greater with sevoflurane (688 mumol/l.h) than with enflurane (591 mumol/l.h). For both groups correlation coefficients were higher for MAC-h and AUC than for MAC-h and peak serum IFC (Figs. 2 and 3). Indices of renal function did not change in either group. DISCUSSION: In our study 1.69 MAC-h sevoflurane produced peak serum IFCs of 34.5 mumol/l. This is in accordance with the investigation of Frink et al. [4], who reported approximately 30 mumol/l after 1.4 MAC-h sevoflurane. Peak serum IFCs with sevoflurane were twice those with enflurane. Within the first 24 h post-anaesthesia, fluoride levels decreased more rapidly after sevoflurane. AUC may be more important than peak serum IFC in evaluating patients who are at risk for renal concentrating defects. In our study there was no evidence of renal dysfunction in either group.

Adult↗
PubMed1996

[The interaction of nitrous oxide and enflurane on the EEG median of 2-3 Hz is additive, but weaker than at 1.0 MAC].

UNLABELLED: The aim of this study was to quantify the interaction of enflurane and nitrous oxide at a constant median EEG frequency. METHODS: Thirty patients were studied during laparotomies. Nitrous oxide was randomly administered in concentrations of 0, 20, 40, 60, and 75 vol.-% for 10 patients for each nitrous oxide concentration. Enflurane vaporizer settings were chosen so that the median EEG frequency was kept constant at 2-3 Hz. The relationship between nitrous oxide concentrations and the required enflurane concentrations was examined with the isobole method. RESULTS: Nitrous oxide decreases the enflurane requirement linearly. Addition of every 10 vol.-% of nitrous oxide decreases the enflurane requirement by 0.042 vol.-%. The total anaesthetic requirement of enflurane and nitrous oxide, expressed in terms of previously reported MAC values, increases significantly with increasing nitrous oxide concentrations. CONCLUSIONS: The interaction of enflurane and nitrous oxide in the dose range from 0 to 75 vol.-% on median EEG frequency is compatible with additivity. The potency of nitrous oxide as a substitute for enflurane is less than might be expected when adding up the MAC values.

Adult↗
PubMedDate not supplied

Recovery following outpatient anesthesia: use of enflurane versus propofol.

STUDY OBJECTIVE: To compare the intraoperative conditions and postoperative recovery of patients following the use of either propofol-nitrous oxide (N2O) or enflurane-N2O for maintenance of outpatient anesthesia. DESIGN: Randomized, single-blind study. SETTING: University hospital outpatient surgery center. PATIENTS: 61 ASA physical status I and II, healthy female outpatients undergoing laparoscopic surgery. INTERVENTIONS: Patients were randomly assigned to one of three anesthetic regimens. Group 1 (control) received thiopental sodium 4 mg/kg intravenously (i.v.), followed by 0.5% to 1.5% enflurane and 67% N2O in oxygen (O2). Group 2 received propofol 2 mg/kg i.v., followed by 0.5% to 1.5% enflurane and 67% N2O in O2. Group 3 received propofol 2 mg/kg i.v., followed by propofol 50 to 160 micrograms/kg/min i.v. and 67% N2O in O2. All patients received succinylcholine 1 mg/kg i.v. to facilitate tracheal intubation and atracurium 10 to 20 mg i.v. to provide adequate relaxation during the maintenance period. MEASUREMENTS AND MAIN RESULTS: Recovery from anesthesia was assessed by a research nurse who was unaware of the anesthetic technique used. The mean +/- SD time to eye opening was significantly longer in the thiopental-enflurane-N2O group (Group 1) than in the propofol-propofol-N2O group (Group 3) (6.1 +/- 2.5 minutes vs. 3.5 +/- 2.8 minutes, respectively). In addition, the mean time to respond to verbal commands was significantly shorter in the propofol induction groups compared with the thiopental induction group. However, the use of enflurane versus propofol for maintenance of anesthesia did not significantly prolong the time from arrival in the recovery room to sitting, tolerating oral fluids, walking, or being judged "fit for discharge." There were no differences among the three groups with respect to postoperative pain or analgesic requirements. Finally, patients who received enflurane for maintenance of anesthesia had a significantly higher frequency of nausea and vomiting than the propofol maintenance group. CONCLUSION: Induction of anesthesia with propofol is associated with a more rapid emergence from anesthesia than induction with thiopental. Maintenance of anesthesia with enflurane did not prolong recovery compared with maintenance with propofol, but enflurane was associated with increased frequency of postoperative nausea and vomiting.

Adult↗
PubMed1996

Effects of enflurane and isoflurane on splanchnic oxygenation in humans.

STUDY OBJECTIVES: To determine the effects of enflurane and isoflurane on hepatic venous oxygen saturation (ShvO2) and splanchnic oxygen (O2) extraction. To measure hemodynamic parameters and ShvO2, mixed venous, and arterial lactate concentrations during enflurane and isoflurane anesthesia. DESIGN: Randomized, prospective study. SETTING: University hospital. PATIENTS: 20 ASA physical status I, II, and III adults, who underwent major abdominal surgery requiring mechanical ventilation a few hours postoperatively. INTERVENTIONS: After placement of catheters in the pulmonary artery, radial artery, peripheral and right hepatic vein, one hour postoperatively either enflurane or isoflurane was applied at different minimum alveolar concentration (MAC) of 0.5, 1.0, and 1.5 in a randomized order. MEASUREMENTS AND MAIN RESULTS: Before and 10 minutes after administration of each desired end-expiratory anesthetic concentration, the following parameters were determined: hemodynamic parameters, arterial (SaO2), mixed venous (SvO2), and hepatic venous oxygen saturations, systemic and splanchnic O2 extraction, arterial, mixed venous, and hepatic venous lactate concentrations. Cardiac output (CO) and mean arterial pressure (MAP) decreased in a dose dependent manner. SaO2, SvO2, and systemic O2 extraction remained unchanged with enflurane and isoflurane anesthesia. In the enflurane group, but not in the isoflurane group, ShvO2 decreased with increasing inhalational concentrations. This decrease in ShvO2 reflected an increase in splanchnic O2 extraction with enflurane; in contrast to isoflurane. CONCLUSIONS: Enflurane causes a decrease in ShvO2, which indicates an impairment of splanchnic perfusion corresponding to the reduction in CO and MAP in a dose-dependent manner. Isoflurane maintains splanchnic perfusion in contrast to enflurane.

Aged↗
PubMed1995

[Rates of awakening, circulatory parameters and side-effects with sevoflurane and enflurane. An open, randomized, comparative phase III study].

OBJECTIVE: Sevoflurane is a "new" volatile inhaled anaesthetic currently undergoing phase III clinical trials in Europe and USA. Owing to the low blood solubility, rapid induction of anaesthesia and emergence from anaesthesia would be expected. In this study, we compared emergence times and haemodynamics in patients receiving either sevoflurane or enflurane. Furthermore, all adverse experiences were recorded, and the relationship to the drug administered was rated. METHODS: Thirty ASA physical status I and II patients were studied in an open, prospective and randomised clinical trial. Anaesthesia was induced with fentanyl, thiopentone and vecuronium for facilitating endotracheal intubation. Anaesthesia was maintained with sevoflurane or enflurane, 60% nitrous oxide in oxygen and additional doses of fentanyl (1-2 micrograms/kg/h). ECG, blood pressure (non-invasive), inspiratory and end-tidal concentrations of sevoflurane or enflurane were monitored continuously. At the end of surgery, administration of sevoflurane or enflurane and nitrous oxide stopped without tapering and emergence times were recorded. All adverse experiences which occurred until the third postoperative day were recorded and the relationship to the inhaled anaesthetic was rated as "none", "unlikely", "possible", "probable" or "highly probable". RESULTS: With the exception of the end-tidal concentration at the end of surgery and the mean inspiratory and end-tidal concentrations, which were higher for sevoflurane, the two patient groups were comparable. Pulmonary elimination was significantly faster and emergence time was significantly shorter (5 vs. 9 minutes) with sevoflurane. Emergence time did not correlate with the duration of anaesthetic exposure (MAC hours) for sevoflurane. There was no difference in the time courses of heart rate and mean arterial blood pressure between sevoflurane and enflurane. No adverse experiences with a "probable" or "highly probable" relationship to the inhaled anaesthetic were observed. CONCLUSION: Emergence time after inhalation anaesthesia depends on (alveolar) ventilation, blood-gas solubility coefficient and, at least for enflurane and isoflurane, on the dose applied (MAC hours). There is no positive correlation between emergence time and dose applied for sevoflurane. Due to the lower blood-gas solubility coefficient (0.6-0.7 for sevoflurane vs. 1.8 for enflurane) pulmonary elimination is faster and emergence time is shorter with sevoflurane. Supplementing inhalation anaesthesia with fentanyl, there is no difference in the time courses of heart rate and mean arterial blood pressure between sevoflurane and enflurane.

Adult↗
PubMedDate not supplied

Biological monitoring of occupational exposure to enflurane (ethrane) in operating room personnel.

Biological monitoring of occupational exposure to enflurane (ethrane) can be achieved by measuring concentrations of inorganic fluorides in the blood and urine and of enflurane in alveolar air and venous blood. Measurement of these concentrations, however, has limitations. Another method for monitoring exposure to enflurane is to measure its concentration in urine throughout the period of exposure. In this study, we measured the environmental and urinary concentrations of enflurane. Enflurane in the ambient atmosphere was determined in 18 operating theaters of eight hospitals in Italy. Ambient air concentrations exceeded the National Institute for Occupational Safety and Health-recommended time-weighted average exposure level of 1 ppm (median: 1.31 ppm). Enflurane was detected in urine of 159 exposed subjects (anesthetists, surgeons, and nurses). A significant correlation was found between enflurane concentration in urine produced during the shift and environmental concentration (r = 0.77, p = .0001). The results showed that urinary enflurane concentration can be used as an appropriate biological exposure index. The biological values proposed are 153 micrograms/l, corresponding to 75 ppm of environmental exposure; 22 micrograms/l, corresponding to 10 ppm of environmental exposure; and 3.5 micrograms/l, corresponding to 1 ppm of environmental exposure. The proposed values can be regarded as time-weighted average samples, reflecting exposure for a 4-h period.

Adult↗