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Attenuation of the cardiovascular intubation response with N2O, halothane or enflurane.

The circulatory intubation response was studied in 75 normotensive, otolaryngological patients after a thiopentone-suxamethonium induction followed by 2 min artificial ventilation with 100% oxygen (control), 70% nitrous oxide in oxygen (N2O), halothane 2% with N2O, enflurane 3% with N2O or enflurane 5% in oxygen. The above study groups (n = 15) were chosen after preliminary experiments performed in 25 different patients with halothane 2% (n = 8) or enflurane 3% (n = 6) in oxygen, which did not prevent the increase of arterial pressure after intubation, or with halothane 3% (n = 11) which attenuated the pressor response but caused cardiac arrhythmias in 55% of patients. Enflurane 5% in oxygen attenuated the increase of systolic arterial pressure by 53%, enflurane 3% with N2O by 34% and halothane 2% with N2O by 31%. The increase in heart rate after intubation was lowest in the halothane 2% with N2O group, but there were no statistically significant differences between the groups. Cardiac arrhythmias were commonest in the enflurane 3% with N2O group (20%) and they did not occur in the halothane 2% with N2O group. Considering the total effect on arterial pressure, heart rate and rate-pressure product, we recommend the combination of halothane 2% with N2O.

Adolescent↗

Cardiac arrhythmias in intubated children during adenoidectomy. A comparison between enflurane and halothane anaesthesia.

In 75 children undergoing adenoidectomy, occurrence of cardiac arrhythmias and influence of anaesthesia on respiration were studied during halothane and enflurane anaesthesia. All the children were intubated orally. In 25 children halothane, and in another 25 children enflurane was used during spontaneous ventilation. Twenty-five children were also followed during halothane anaesthesia with manually controlled ventilation. The overall incidence of cardiac arrhythmias was higher during halothane anaesthesia (72% at spontaneous breathing and 68% with controlled ventilation) than during enflurane anaesthesia (32%, P less than 0.05). Ventricular arrhythmias were noted in 20% of the spontaneously breathing children in 12% of those with controlled ventilation during halothane anaesthesia. Three children breathing spontaneously during halothane anaesthesia developed ventricular tachycardia. During enflurane anaesthesia the incidence of ventricular arrhythmias was lower (8%) in spite of higher end-tidal CO2 tensions and an anaesthetic depth that was only just the level needed to allow intubation. The incidence of ventricular arrhythmia during halothane anaesthesia was shown to be influenced by the anaesthetic technique used, which was not found with enflurane anaesthesia. The greater stability in cardiac rhythm with enflurane indicates a more favourable effect of this agent on the myocardium as well as a decreased sympathetic response to anaesthesia and surgery as compared with halothane anaesthesia.

Adenoidectomy↗

Intestinal vascular effects of inhaled and locally administered enflurane in the cat.

The effects of enflurane on intestinal vascular resistance and blood flow in the intestine were studied in cats during basal chloralose anaesthesia. A jejunal segment was prepared and perfused with blood from both femoral arteries, allowing control of intestinal inflow pressure. Mesenteric venous blood flow was measured with an optical drop recorder. During constant intestinal arterial pressure (75 mmHg; 10 kPa), intestinal vascular resistance was calculated during enflurane inhalation at MAC 0.5 and 1.0 before and after postganglionic denervation of the jejunal segment. Inhalation of enflurane reduced intestinal vascular resistance in a dose-dependent fashion. The decrease in vascular resistance was attenuated but not abolished by post-ganglionic denervation, indicating both peripheral and central nervous sites of action for enflurane. Furthermore, with the intestinal segment perfused at systemic arterial pressure, the effects of locally intraarterially infused enflurane dissolved in a fat emulsion was studied. A vasodilator response was elicited in the intestine when exposed to local arterial enflurane concentrations in the same range as encountered during surgical anaesthesia in man, supporting the hypothesis of a peripheral site of action.

Anesthesia, Inhalation↗

Enflurane inhibits muscle fasciculations caused by suxamethonium in children.

Eighty-three children with a mean age of 2.7 years were anaesthetized with either thiopental 5 mg/kg followed by suxamethonium 1.5 mg/kg i.v. or with enflurane 5 vol% in 70% nitrous oxide in oxygen via a face mask. In the enflurane group, venepuncture was performed when the children were unconscious, 1.8 +/- 0.05 (s.e.) min after the start of anaesthesia. After enflurane, suxamethonium 1, 1.5 or 2 mg/kg was administered i.v. for endotracheal intubation. The incidence and duration of muscle fasciculations after suxamethonium were significantly lower (P less than 0.01) in the enflurane groups than in the thiopental group. The fasciculation index was significantly lower (P less than 0.01) in the enflurane groups than in the thiopental group. In the enflurane groups, intubating conditions were better (P less than 0.05) in the children treated with suxamethonium 2 mg/kg than in those treated with suxamethonium 1 mg/kg.

Child↗

Halothane, enflurane and isoflurane anaesthesia for adenoidectomy in children, using two different premedications.

In 48 children subjected to adenoidectomy, comparisons of airway problems, heart rates, cardiac arrhythmias, ventilation and stress hormone reactions were studied during halothane, enflurane and isoflurane anaesthesia. Sixteen children were anaesthetized with either of the three agents and eight patients in each group received diazepam 0.25 mg kg-1 and atropine 0.015 mg kg-1 rectally (DA) as premedication and the remainder diazepam 0.5 mg kg-1, morphine 0.15 mg kg-1 and scopolamine 0.01 mg kg-1 (DMS) rectally. All children were intubated and breathing spontaneously. Equianaesthetic inspired concentrations of halothane, enflurane and isoflurane were used. Airway problems were of the same magnitude during halothane and isoflurane anaesthesia but were less frequent with both agents compared with enflurane anaesthesia. DMS reduced the number of airway reactions in all groups. Respiratory rates were uninfluenced by anaesthesia, intubation and surgery during enflurane anaesthesia. Cardiac arrhythmias were less frequent with enflurane and isoflurane than with halothane. Plasma ACTH and cortisol were similar with all three agents. During induction of anaesthesia in the DA-premedicated halothane group, however, plasma catecholamines were higher than in the group which received DMS, in contrast to the findings during enflurane and isoflurane anaesthesia. The DMS premedication decreased the response of plasma ACTH, cortisol and plasma catecholamines to surgery.

Adenoidectomy↗

Vomiting, retching, headache and restlessness after halothane-, isoflurane- and enflurane-based anaesthesia. An analysis of pooled data following ear, nose, throat and eye surgery.

BACKGROUND: Isoflurane has exceeded halothane and enflurane in usage. A literature search, however, revealed no data comparing the effects on emesis, headache and restlessness of these three agents. METHODS: With hospital ethics committee approval and patient consent, a prospective, randomised, double-blind study of 556 patients undergoing ENT and eye surgery was undertaken to evaluate the effects of halothane, isoflurane and enflurane on vomiting, retching, headache and restlessness until 24 h after anaesthesia. Balanced general anaesthesia was administered comprising benzodiazepine premedication, induction with thiopentone-atracurium-morphine (ENT patients) or fentanyl (eye patients), controlled ventilation and maintenance with either halothane 0.4-0.6 vol% (n = 186), isoflurane 0.6-0.8 vol% (n = 184) or enflurane 0.8-1 vol% (n = 186) in nitrous oxide 67% and oxygen. RESULTS: The three study groups were comparable, and comprised comparable subgroups having ear, nose, throat, intraocular and non-intraocular surgery. During early recovery from anaesthesia, the respective requirements for halothane, isoflurane and enflurane for analgesia (7%, 9% and 10%), frequency of emesis (6%, 8% and 8%), antiemetic requirements (1%, 1% and 2%), restlessness-pain scores and time spent in the recovery ward (27 SD 10, 31 SD 12 and 26 SD 9 min) were similar. During the ensuing 24-h postoperative period, patients who had isoflurane experienced emesis less often than those who had halothane (36% vs 46%, P < 0.025) but did so with similar frequency to those who had enflurane (46% vs 41%). Antiemetic requirements were least in those given isoflurane (isoflurane 12%, halothane and enflurane 23% each, P < 0.005), but headache and analgesic requirements were similar. CONCLUSION: Isoflurane induces less postoperative emesis than halothane, but headache is similarly frequent after anaesthesia with any of these agents.

Adult↗

Possible participation of NMDA and glycine receptors but not GABAA receptors in enflurane-induced opisthotonus in mice.

1. We previously reported that volatile anaesthetics produce incidences of a transient opisthotonus in mice, a sign of CNS stimulation. This study was performed to investigate mechanisms by which enflurane-induced opisthotonus (EIO) occurs. 2. The effects of pretreatment of N-methyl-D-aspartate (NMDA) antagonists dizocilpine (MK-801; DIZ) and ketamine (KET), GABAA antagonists picrotoxin (PIC), pentylenetetrazol (PTZ) and glycine antagonist strychnine (STR) on the incidence of EIO were determined. Prior to exposure to 2.0% enflurane in air, male ddN mice were given intraperitoneal injections of 0.2 mL saline (control), 0.5-5.0 mg/kg DIZ, 20-80 mg/kg KET, 2.9 mg/kg PIC, 40.0 mg/kg PTZ and 0.75 mg/kg STR. After the injection, the behavioural state of the mice was observed for 20 min (the pre-enflurane period). During the exposure to enflurane the time for immobilization, that is, anaesthetic induction time (IT), and the incidence of EIO were measured. 3. Dizocilpine (1.0-5.0 mg/kg) and KET (80 mg/kg) significantly (P < 0.01) reduced both the incidence of EIO and IT in a dose-dependent manner. During the pre-enflurane period DIZ produced incidences (5-40%) of transient seizures in a dose-dependent manner, while KET did not induce them at all. The two GABAA antagonists had no detectable effect on the EIO. Strychnine significantly enhanced the EIO. These CNS stimulants resulted in a 3-10% incidence of transient seizure and/or opisthotonus during the pre-enflurane period, but there was no correlation between DIZ-induced seizure and EIO. 4. These results suggest that the EIO is mediated by the NMDA and the STR-sensitive glycine receptors, but not the GABAA receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of halothane, enflurane, and isoflurane on supraventricular and ventricular rate in dogs with complete atrioventricular block.

Complete atrioventricular (AV) block was produced in 32 chloralose-anesthetized autonomically intact dogs to determine the effects of halothane, enflurane, and isoflurane on supraventricular and ventricular rate. Halothane (n = 17), enflurane (n = 6), and isoflurane (n = 9) were administered in three separate experiments in sequential minimum alveolar concentration (MAC) multiples of 0.5, 1.0, 1.5, 2.0, 1.5, and 1.0. Supraventricular rate, ventricular rate, and mean arterial blood pressure (MAP) were measured and recorded at baseline and after a 20-minute equilibration period of each inhalation anesthetic at each MAC multiple. Increasing concentrations of enflurane and isoflurane significantly decreased supraventricular rate (P < .05). Ventricular rate was not significantly changed by sequential MAC multiples of halothane, enflurane, and isoflurane. Increasing concentrations of halothane, enflurane, and isoflurane significantly decreased MAP with enflurane producing the most significant decrease (P < .05). Ventricular arrhythmias occurred in 5 of 17 dogs anesthetized with halothane and 1 of 9 dogs anesthetized with isoflurane. Inhalation anesthesia can significantly decrease supraventricular rate and MAP, does not alter ventricular rate, and can produce ventricular arrhythmias in dogs with complete AV block.

Anesthesia, Inhalation↗

Effect of isoflurane and enflurane on the electrocorticogram of epileptic patients.

We studied the effect of inhaled anesthetic agents on the electrocorticogram (ECoG) in four epileptic patients during nondominant right hemisphere temporal lobectomy while they received 70% nitrous oxide in oxygen (70% N2O/O2) alone, 70% N2O/O2 with 0.5 to 1.5% isoflurane, or 70% N2O/O2 with 2% enflurane. The mean frequency of epileptiform spikes decreased during use of isoflurane, but not enflurane, compared with use of 70% N2O/O2 alone. Enflurane produced paroxysms of synchronous high-voltage spikes. The mean number of electrodes exhibiting spike activity decreased with isoflurane use and increased with enflurane use compared with use of 70% N2O/O2 alone. This preliminary study suggests that isoflurane can suppress epileptogenic tissue and that both isoflurane and enflurane can distort the ECoG, confounding accurate identification of the seizure focus. When used judiciously, however, enflurane may be a potent synchronizer and activator of the epileptogenic focus, making it easier to identify.

Action Potentials↗

Enflurane and uterine contractility in rabbits.

The effect of enflurane on uterine contractility was studied in sexually mature rabbits in which intrauterine balloon catheters had been implanted. Three animal groups were studied: untreated; treated with estrogen-progesterone; and 27 to 28 days pregnant. The effects of 1.5 percent or 3.0 percent enflurane were quantitated by measuring contraction frequency and amplitude during an anesthetically steady state. The effects of prior anesthesia with 1.5 percent enflurane on uterine responses to 1.5 IU oxytocin IV were also evaluated. Neither 1.5 percent of 3.0 percent enflurane altered contraction amplitude or frequency in the 3 groups of rabbits. However, the amplitude of the contractile response to oxytocin 30 minutes following enfluane was significantly depressed. The results indicate that, while the intact rabbit uterus under different hormonal influences is not depressed by 1.5 or 3.0 percent enflurane, its response to oxytocin following enflurane is decreased.

Animals↗

Effect of enflurane on contractile reactivity in isolated canine mesenteric arteries and veins.

The effects of enflurane on responses of isolated canine mesenteric arteries and veins to transmural nerve stimulation and to exogenously administered norepinephrine (a mixed alpha 1- and alpha 2-adrenoceptor agonist), phenylephrine (a selective alpha 1-adrenoceptor agonist), and tyramine were studied. The contractile responses of the arteries and the veins to transmural nerve stimulation and to norepinephrine were attenuated by exposure to enflurane; the responses to phenylephrine were decreased more than those to norepinephrine. When compared with the effect of enflurane on transmural nerve stimulation-induced responses, exposure to enflurane resulted in slight attenuation of the contractile responses caused by tyramine, suggesting that enflurane may inhibit the responses to tyramine by interfering with an interaction between released norepinephrine and postjunctional alpha 1-adrenoceptors rather than with tyramine-induced norepinephrine release. The data are also consistent with the view that enflurane acts on sympathetic nerve endings to inhibit release of norepinephrine associated with electrical stimulation-induced nerve membrane depolarization.

Animals↗

Cardiac electrophysiologic effects of diltiazem in dogs receiving either enflurane or chloralose anesthesia.

Previously we have described impaired myocardial conduction in patients receiving diltiazem and enflurane. The present study examines the possible mechanism(s) which may account for our clinical observation and presents methods of reversing adverse interactions. Nineteen mongrel dogs were randomized into two exposure groups: enflurane or chloralose anesthesia. Stepwise increasing doses of diltiazem were administered until predetermined endpoints were reached. Sinus and atrioventricular (AV) node function was assessed at all levels of diltiazem infusions, and after reversal drugs. Depression of AV nodal conduction and refractoriness after diltiazem administration was greater during enflurane anesthesia when compared with chloralose. There was severe sinus node dysfunction in enflurane-anesthetized animals. These effects were only reversed by isoproterenol. Patients may be at increased risk for severe sinus node depression when diltiazem is administered during enflurane anesthesia. This is due to a potent interaction between diltiazem and enflurane on the sinoatrial node.

Anesthesia, Inhalation↗

The effects of enflurane, isoflurane, and intravenous anesthetics on rat diaphragmatic function and fatigability.

UNLABELLED: We examined the effect of isoflurane, enflurane, midazolam, ketamine, propofol, and thiopental on diaphragmatic functions under unfatigued and fatigued conditions in 228 rat isolated muscle strips. Diaphragmatic twitch characteristics and tetanic contractions were measured before and after muscle fatigue, which was induced by repetitive tetanic contraction with or without exposure to one of the anesthetics at clinically relevant plasma concentrations, and at 10 and 100 times this concentration, or at 1, 2, and 3 minimum alveolar anesthetic concentration (MAC). Isoflurane, midazolam, ketamine, propofol, and thiopental did not induce a direct inotropic or lusitropic effect under unfatigued and fatigued conditions. Enflurane did not change contraction or relaxation in fresh isolated diaphragm, but enflurane at 2-3 MAC enhanced diaphragmatic fatigability itself and fatigue-induced impairment of twitch characteristics and tetanic tensions. These effects were greater at 3 MAC than at 2 MAC. Our findings suggest that the reduction of diaphragm function previously reported in in vivo experiments using propofol, midazolam, and isoflurane is not related to a direct effect on intrinsic diaphragmatic contractility. Our results also indicate that large concentrations of enflurane may impair the diaphragmatic function at sites other than excitation-contraction coupling. IMPLICATIONS: Enflurane did not change contraction or relaxation in fresh isolated rat diaphragm, but enhanced diaphragmatic fatigability itself and fatigue-induced impairment of twitch characteristics and tetanic tensions. Isoflurane, midazolam, ketamine, propofol, and thiopental had no direct effects on diaphragmatic functions under unfatigued and fatigued conditions. Isoflurane and these i.v. anesthetics may be advantageous over enflurane to anesthetize and/or sedate patients who are predisposed to diaphragmatic fatigue.

Anesthetics, Inhalation↗

[Effects of enflurane on the elastic properties of frog skinned skeletal muscle fiber under relaxed and rigor conditions].

We studied the effects of enflurane on the elastic property of the mechanical skinned fiber prepared from M. Semitendinosus of bullfrog. Longitudinal and lateral elastic properties of the skinned fibers were measured under relaxed and rigor conditions to clarify the effects of enflurane on actomyosin complex. Under the rigor condition, enflurane did not change the lateral elasticity of the fibers, but enflurane decreased the longitudinal elasticity. On the other hand, under the relaxed condition, enflurane did not change the elasticity. The results suggest that enflurane probably decreases the force of binding of cross-bridges to actin, which is one of the factors to reduce the maximal force.

Animals↗

[Ventilatory effects of halothane and enflurane in dogs].

The ventilatory effects of halothane and enflurane were studied in permanently tracheostomized dogs at the same anesthetic depth of 1 MAC. Inspiratory and expiratory durations were longer and tidal volume greater during enflurane than during halothane anesthesia. Mean inspiratory flow rate and minute ventilation during enflurane anesthesia were less than those during halothane anesthesia. As a result, end-expiratory carbon-dioxide concentration was higher during enflurane than during halothane anesthesia. When end-expiratory carbon-dioxide concentration was held at 7.5%, tidal volume was not different between the two anesthetics, while the difference of other parameters still remained. In addition, the magnitude of Hering-Breuer reflex determined by end-expiratory airway occlusion was essentially identical between halothane and enflurane anesthesia. The present results indicate that 1) depressant effect of enflurane on respiratory drive is greater than that of halothane and 2) the two anesthetics act on the respiratory timing mechanism differently.

Animals↗

Fatal accidental enflurane intoxication.

Among reported cases of abuse of volatile anesthetics there is only one of enflurane intoxication. We report another fatal enflurane intoxication. A 21-year-old man found dead seemed to have experimented with enflurane. Three and one-half days after death high amounts of enflurane were detected in blood, brain, and subcutaneous fat. Gas chromatographic quantification revealed the following high enflurane concentrations: blood: 130 mg/l-1, brain: 350 mg/l-1, and subcutaneous fat: 100 mg/l-1. Histologic signs of drug-induced damage were lacking. No suicide intentions became known. It was concluded that the young man died of an accidental intoxication while abusing enflurane.

Adult↗

Comparison of arterial baroreflex function in humans anesthetized with enflurane or isoflurane.

To compare the depressive effects of isoflurane and enflurane on the arterial baroreflex function, we examined baroreflex control of heart rate during the entire course of clinical anesthesia. Isoflurane and enflurane were found to have similar depressive effects on the baroreflex control of heart rate when used in combination with N2O and O2. Suppression in the baroreflex sensitivity, defined by the slopes of regression line (change in msec of RR interval per mm Hg increase or decrease in systolic blood pressure) was from 7.1 +/- 3.9 to 1.8 +/- 0.7 msec/mm Hg in patients given isoflurane and from 7.8 +/- 4.3 to 3.0 +/- 1.9 msec/mm Hg in those given enflurane when evaluated by a pressor test (bolus IV phenylephrine). The slope of the depressor test (bolus IV nitroglycerin) also decreased from 4.7 +/- 2.8 to 1.9 +/- 1.5 msec/mm Hg with isoflurane and from 5.6 +/- 3.2 to 2.3 +/- 1.2 msec/mm Hg with enflurane. During surgery in which anesthetic concentration invariably needed to be increased, the suppression of the baroreflex sensitivity remained unchanged in both groups of patients. During recovery, the arterial baroreflex function in patients given isoflurane recovered more rapidly than that in patients given enflurane. This difference may be related to a more minor degree of suppression of isoflurane on the autonomic nervous system compared to enflurane.

Adult↗

Effects of halothane, isoflurane and enflurane on isolated rat heart muscle.

Since the effects in the intact organism are complicated by central as well as peripheral effects, we compared the direct cardiac effects of three commonly used inhalational anaesthetics--halothane, isoflurane and enflurane--on isolated heart muscle. Concentration-response curves for inotropic, chronotropic and ventricular automaticity effects of halothane, isoflurane and enflurane (0.1-2% v/v) on electrically stimulated left atria, right atria and right ventricles of the rat were obtained. All three inhalational anaesthetics significantly decreased contractile force; the inhibitory concentration 50 (IC50) of enflurane was 0.55 +/- 0.06% v/v, significantly lower than halothane (0.96 +/- 0.08% v/v) and isoflurane (0.67 +/- 0.05% v/v). Similar results were obtained on atrial nomotopic rate. Halothane, isoflurane and enflurane produced negative chronotropic effects in this preparation. On the other hand, halothane and isoflurane significantly reduced the ventricular ectopic automaticity. However enflurane (0.3, 0.5, 1% v/v) increased ventricular rate. There were statistically significant differences between the IC50 values of atrial and ventricular rate for halothane and isoflurane. These results indicate: (a) direct negative inotropic and chronotropic effects for the three inhalational anaesthetics tested; (b) anti-dysrhythmic actions for halothane and isoflurane; and (c) dysrhythmogenic effects of enflurane.

Animals↗