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PubMed1998

Effect of halothane in cortical cell cultures exposed to N-methyl-D-aspartate.

In vivo studies have shown potent protection by volatile anesthetic agents against cerebral ischemic insults. Volatile agents have also been shown to antagonize glutamatergic neurotransmission at the N-methyl-D-aspartate (NMDA) receptor. This study examined the potential for halothane to reduce neuronal excitotoxic lesions caused by NMDA. Fetal rat cortical cell cultures were allowed to mature 13-16 d. Culture wells (n = 13-16) were treated with 0 mM - 3.96 mM halothane in the presence/absence of 30 microM NMDA. Additional cultures were exposed to 30 microM NMDA in the presence/absence of 10 microM MK-801 or 10 microM ACEA 1021. Cellular lethality was assessed by measurement of lactate dehydrogenase (LDH) 24 hrs later. A maximal effect of halothane was observed at 0.70 mM (2.1 vol%) wherein a 36% reduction in NMDA-stimulated LDH release occurred relative to untreated controls. Both MK-801 and ACEA 1021 caused complete inhibition of NMDA-stimulated LDH release. These data confirm that halothane has modulatory effects at the NMDA receptor but potency of this drug is less than that of specific antagonists of either glutamate or glycine. These findings suggest that halothane protection in vivo can be partially explained by anti-excitotoxic properties although other mechanisms of action are probably also important.

Animals↗
PubMed2000

Recovery characteristics of sevoflurane or halothane for day-case anaesthesia in children aged 1-3 years.

BACKGROUND: Our objective was to compare the recovery characteristics of sevoflurane and halothane for short day-case anaesthesia in a specifically limited age group of children 1-3 yr. METHODS: Eighty unpremedicated children undergoing day-case adenoidectomy were randomly assigned to receive inhalational induction with either sevoflurane 8% or halothane 5% and nitrous oxide in oxygen (70/30) via a face mask. Tracheal intubation was performed without a muscle relaxant. Anaesthesia was continued with the volatile anaesthetic, adjusted to maintain heart rate and blood pressure within +/-20% of initial values. Recovery was evaluated using a modified Aldrete score, a Pain/Discomfort scale and by measuring recovery end-points. A postoperative questionnaire was used to determine the well-being of the child at home until 24 h after discharge. RESULTS: Emergence and interaction occurred significantly earlier after sevoflurane than halothane but discharge times were similar. More children in the sevoflurane group achieved full Aldrete scores within the first 30 min after anaesthesia, although this group suffered more discomfort during the first 10 min. The amount of postoperative analgesic administered was higher and the first dose given earlier in the sevoflurane group. Postoperative vomiting was more common with halothane, but side-effects in the two groups were otherwise similar in the recovery room and at home. CONCLUSIONS: In children 1-3 yr, sevoflurane provided more rapid early recovery but not discharge after anaesthesia of <30-min duration. Apart from more vomiting with halothane and more discomfort during the first 10 min after awakening with sevoflurane, the quality of recovery was similar with the two anaesthestics.

Ambulatory Surgical Procedures↗
PubMed2001

The influence of halothane, isoflurane and sevoflurane on rocuronium infusion in children.

BACKGROUND: Rocuronium is a non-depolarizing neuromuscular blocking agent with intermediate duration of action and without significant cumulative properties, suitable for continuous infusion. This study was designed to determine the infusion requirements in children under nitrous oxide and fentanyl, halothane, isoflurane or sevoflurane anaesthesia. METHODS: Forty children, 3-11 years old, ASA physical status group I or II were studied. They were randomly allocated to receive fentanyl-nitrous oxide, 1 MAC halothane-nitrous oxide, 1 MAC isoflurane-nitrous oxide or 1 MAC sevoflurane-nitrous oxide anaesthesia. Rocuronium, 0.6 mg(-1) was used to facilitate endotracheal intubation. Electromyographic response of adductor pollicis to train-of-four (TOF) stimulation, 2 Hz for 2 s, applied to the ulnar nerve at 10-s intervals was recorded using Relaxograph (Datex, Helsinki, Finland). Once the first twitch response (T1) returned to 5%, muscle relaxation was maintained by continuous infusion of rocuronium, adjusted automatically in a closed-loop system to maintain a stable 90-99% T1 depression. The block was considered stable if it changed by no more than 2% over a 10-min observation period. RESULTS: Halothane, isoflurane and sevoflurane groups had ower infusion requirements than the fentanyl-nitrous oxide group (P<0.00075). Rocuronium requirement (mean +/- SD) at one hour from the commencement of anaesthesia was 16.7+/-2.3, 13.6+/-3.7, 13.1+/-5.1 and 8.4+/-1.6 microg x kg(-1) x min(-1) for children receiving fentanyl-nitrous oxide, halothane, isoflurane and sevoflurane anaesthesia, respectively. CONCLUSIONS: The rocuronium infusion rate required to maintain stable 90-99% T1 depression was reduced by approximately 20% with halothane and isoflurane anaesthesia, and by 50% with evoflurane anaesthesia when compared to fentanyl-nitrous oxide anaesthesia. Significant patient-to-patient variability of infusion rate makes monitoring of neuromuscular transmission necessary.

Adjuvants, Anesthesia↗
PubMed2000

Sodium channel isoform-specific effects of halothane: protein kinase C co-expression and slow inactivation gating.

The modulatory effect of protein kinase C (PKC) on the response of Xenopus oocyte-expressed Na channel alpha-subunits to halothane (2-bromo-2-chloro-1,1,1-trifluroethane) was studied. Na currents through rat skeletal muscle, rat brain and human cardiac muscle Na channels were assessed using cell-attached patch clamp recordings. PKC activity was increased by co-expression of a constitutively active PKC alpha-isozyme. Decay of macroscopic Na currents could be separated into fast and slow exponential phases. PKC co-expression alone slowed Na current decay in neuronal channels, through enhancement of the amplitude of the slower phase of decay. Halothane (1.0 mM) was without effect on any of the three isoforms expressed alone but, after co-expression of PKC, there was enhancement of Na current decay with reduction in charge movement through skeletal muscle and neuronal channels. Cardiac channels were relatively insensitive to halothane. Enhanced Na current decay resulted from suppression of the slow phase, without effect on the faster phase or on either decay tau. Suppression of Na current through skeletal muscle channels was concentration-dependent over the therapeutic range and was described by third order reaction kinetics, with an IC(50) of 0.55 mM. We conclude that the halothane suppresses skeletal muscle and brain Na channel activity in this preparation through a reduction in the slow mode of inactivation gating, but only after PKC co-expression. Cardiac Na channels were relatively insensitive to halothane. The mechanism is likely to involve phosphorylation of the channel inactivation gate, although phosphorylation of other sites in the channel may account for the isoform specific differences.

Animals↗
PubMed1993

Fast-responding, fibre-optic based sensing system for the volatile anaesthetic halothane, using an ultraviolet absorption technique and a fluorescent film.

An improved version of a fast-responding sensing system for the widely used volatile anaesthetic halothane (2-bromo-2-iodo-1,1,1-trifluoroethane) is described. The concentration of halothane is determined using an ultraviolet radiation (UV) absorption technique. Ultraviolet radiation at 230 nm is conveyed by a silica optical fibre to a gas flow-through cell containing the halothane, and the intensity of the UV reaching the other side of the cell is measured using a fluorescent polymer film. This paper describes the development of an efficient fluorescent polymer film for the sensor based on poly(ethylene glycol) containing two fluorophores (2,5-diphenyloxazole and tris[4,4,4-trifluoro-1-(2-thienyl)butane- 1,3-diono]europium(III)). The film fluoresces strongly with a red line spectrum when excited in the range from about 200 to 380 nm. There is evidence of direct energy transfer between the two fluorophores. A similar effect is observed in films prepared from Carbowax 20M and the europium chelate. An advantage of this approach is that the fluorescent radiation can be transmitted back to a silicon photo-detector using an inexpensive polymer optical fibre bundle. Two experimental sensor systems for halothane are described and the results show that, although the response does not obey the Beer-Lambert law, a reliable system for determining halothane can be constructed, which operates over the medically important range 0-3%. This paper also describes how the signal-to-noise ratio of the system can be improved by using the long fluorescence lifetime of the film.(ABSTRACT TRUNCATED AT 250 WORDS)

Chemistry Techniques, Analytical↗
PubMed2000

The effect of low concentrations of halothane on the cerebrovascular circulation in young children.

To determine the effect of halothane on cerebral blood flow velocity measured by transcranial Doppler, 23 healthy young children were studied during surgery. Anaesthesia was induced with thiopental, fentanyl and vecuronium, and maintained with halothane in 70% nitrous oxide in oxygen. A continuous epidural anaesthesia with 0. 25% bupivacaine was performed. End-tidal carbon dioxide pressure, temperature, heart rate and systolic blood pressure were kept constant. Three minimal alveolar concentrations (MAC; 0.5, 1.0 and 1. 5) of halothane were administered in stepwise increases. The cerebral blood flow velocity increased significantly at 1.0 (p < 0. 01) and 1.5 MAC (p < 0.001) compared with the value at 0.5 MAC. No further change in cerebral blood flow velocity was seen between 1.0 and 1.5 MAC. These data show that maximal changes in cerebral blood flow velocity are obtained at 1.0 MAC and that further increases in halothane concentration do not modify the cerebral circulation. It is suggested that young children differ from adults in that the maximal effect of halothane occurs at lower concentrations.

Anesthetics, Inhalation↗
PubMed1999

Effects of theophylline on human cerebral blood flow velocity during halothane and isoflurane anaesthesia.

The acute influence of therapeutic doses of theophylline on cerebral blood flow velocities during general anaesthesia induced either by halothane or isoflurane has not been elucidated previously. The aim of this study, was therefore to investigate these effects during steady state anaesthetic conditions in anaesthetized patients using transcranial Doppler sonography. Thirty-four Patients were investigated. Anaesthesia was maintained either with 1 MAC (minimum alveolar concentration) halothane (n = 16) or 1 MAC isoflurane (n = 18); FiO2: 40%; end-expiratory pCO2: normocapnia. Theophylline administration was performed before surgery by infusing 6 mg kg-1 over a period of 7.5 min. Measurements were recorded prior to theophylline administration, and immediately after 2 mg kg-1 (2.5 min), 4 mg kg-1 (5 min) and 6 mg kg-1 (7.5 min), as well as 5, 10, 15, 20, 30 and 45 min after theophylline administration. Recorded variables included blood pressure, heart rate, arterial oxygen saturation, end-expiratory pCO2, body temperatures, middle cerebral artery blood flow velocity and pulsatility index. Theophylline administration was well tolerated by all study subjects. Heart rate, blood pressure, body temperatures, arterial oxygen saturation and end-expiratory pCO2 remained constant during the whole examination period. Following theophylline, mean blood flow velocity decreased by 25% in the halothane and by 30% in the isoflurane group (P < 0.05). By the end of the examination period, mean blood flow velocity had not yet recovered to the initial values whereby in both groups the mean blood flow velocity was 26% below the initial values. In the isoflurane group, the pulsatility index increased by about 20% (P < 0.05) and remained high until the end of the examination. In the halothane group, however, there were no changes in the pulsatility index. Our results show a remarkable, significant and simultaneous decrease in blood flow velocity in the middle cerebral artery associated with theophylline administration during halothane and isoflurane anaesthesia in man.

Adult↗
PubMed2003

Comparison of electroencephalogram activity and auditory evoked responses during isoflurane and halothane anaesthesia in the rat.

OBJECTIVES: To compare the second differential index (SDI) calculated from the auditory evoked potential (AEP) and electroencephalogram (EEG) parameters: median frequency (MF), spectral edge frequency (SEF) and burst suppression rate (BSR) determined at four equivalent minimum alveolar concentrations (MAC) of isoflurane or halothane. ANIMALS: Twelve male Wistar rats weighing 418 g (SD +/- 18.4 g). METHODS: Auditory evoked potentials and EEG responses were recorded in animals implanted with electrodes at established anaesthetic concentrations. Depth of anaesthesia was assessed using the strength of the pedal withdrawal reflex (PWR), and data were analysed using repeated measures anova and paired t-tests. RESULTS: The SEF tended to decrease with increasing depth of halothane anaesthesia (F = 4.198, p = 0.05), but not with isoflurane. The MF and SDI were significantly higher during halothane than with isoflurane (F = 5.82, p = 0.036 and F = 5.263, p = 0.045, respectively) at equivalent depths of anaesthesia, and EEG burst suppression occurred at deeper planes of isoflurane but not halothane anaesthesia. CONCLUSIONS: The study demonstrated that EEG and AEP characteristics recorded at MAC equivalent concentrations were suppressed to a greater degree by isoflurane than by halothane. These findings have strong implications for research projects where EEG recordings are collected, and also cast more general doubts upon the value of such parameters for evaluating depth of isoflurane anaesthesia in rats.

Anesthesia, Inhalation↗
PubMed1992

[Effect of the volatile anesthetics halothane, enflurane and isoflurane on liver circulation in the human].

In 40 patients with normal liver function total hepatic blood flow (HBF) was determined by the indocyanine-green clearance method simultaneously with haemodynamic parameters, including cardiac output by means of the noninvasive thoracic electrical bioimpedance method. Furthermore, the influence of halothane, enflurane or isoflurane on HBF and the interaction with haemodynamic parameters was studied. HBF and the cardiocirculatory parameters were determined under normal conditions (waking state) and the 40 patients were then divided into 4 groups (each n = 10). After standardised induction of anaesthesia (0.3 mg/kg etomidate and 2 micrograms/kg fentanyl) and tracheal intubation (1.5 mg/kg suxamethonium chloride) an inhalation anaesthesia in O2/air under control of normal end tidal carbon dioxide concentration was performed by intermittent positive pressure ventilation. Anaesthesia was maintained in the 4 groups either with 1 MAC halothane, 1 MAC enflurane, 1 MAC isoflurane or 1.3 MAC isoflurane. The measurements were repeated at a steady of the desired end expiratory concentration of the respective volatile anaesthetic. All three anaesthetics produced a significant and comparable decrease of cardiac output and arterial blood pressure. Differences between halothane, enflurane and isoflurane in respect of haemodynamic parameters were only minimal. Contrariwise, marked differences could be seen in the effects of the anaesthetics on HBF. In the presence of halothane and enflurane HBF dropped to 58% and 56% resp. of the control value, whereas during isoflurane anaesthesia HBF remained unchanged. Furthermore, only during halothane anaesthesia a significant correlation between arterial blood pressure and HBF could be observed indicating a loss of autoregulation of the hepatic blood flow.

Adolescent↗
PubMed1994

[Effect of halothane anesthesia on cerebral blood flow velocity in children].

The effects of halothane on the cerebral circulation were studied in 23 children during general anaesthesia. Blood flow velocity in one middle cerebral artery was recorded continuously by transcranial Doppler sonography. Furthermore arterial blood pressure, pulse rate, endtidal CO2partial pressure and endtidal halothane concentration were recorded. Mean flow velocities/mean arterial blood pressures were 79 cm x s-1/65 mmHg; 86 cm x s-1/61 mmHg; 78 cm x s-1/54 mmHg and 67 cm x s-1/48 mmHg with 1; 1.5; 2 and 2.5 per cent endtidal halothane concentrations, respectively. Endtidal CO2-partial pressure and pulse rate remained constant throughout the study. The higher cerebral blood flow velocities seen with 1.5 per cent halothane compared with 1 per cent can be explained by an increase in cerebral blood flow. The lower cerebral blood flow velocities and arterial blood pressure with 2.5 per cent halothane compared with 1.5 per cent indicate impaired cerebral autoregulation. However, cerebral blood flow appeared to be sufficient even with low arterial blood pressures.

Anesthesia, General↗
PubMed1997

[Echocardiography values in the halothane uptake phase--measurement by acoustic quantification and manual evaluation].

In 35 ASA group I and II patients we investigated the influence of haemodynamic changes induced by increasing concentrations of halothane (from 0.0 to 0.6% halothane in 70% N20) on parameters of transesophageal echocardiography (TEE). Measurements by TEE were taken in manual and automatic boundary detection mode. In manual mode the left ventricular endsystolic area (ESA) increased significantly (+16.3%) and the fractional area change (FAC) decreased significantly (-14.9%). There was no significant change of left ventricular end diastolic area (EDA). In the automatic mode there was a significant increase of ESA and EDA (+13.8%; +6.0%) and a significant decrease of FAC (-10.9%). Peak ejection rate (PER) and peak filling rate (PFR) which were also assessed in automated mode decreased significantly (-10.0%; -5.7%) under halothane. No change occurred with manually determined left ventricular endsystolic wall stress (LVEWS). The endsystolic quotient decreased significantly both in manual and automated mode during halothane (-28.3%; -29.9%). No significant difference existed between TEE measurements under apnoea versus under controlled ventilation (except for EDA in automated mode). We conclude that there is no need for apnoea conditions for TEE measurements. In conclusion, TEE proves a useful monitoring system in anesthesia which enables the investigator to assess the negative inotropic effect of halothane. Problems in its practical usage are due to the wide variation of TEE measurements.

Adult↗
PubMed1985

Halothane hepatitis. Detection of a constitutional susceptibility factor.

We studied susceptibility to halothane hepatitis with an in vitro test that detects cell damage from electrophilic drug intermediates. Metabolites of phenytoin were generated by incubation of phenytoin with rat hepatic microsomes in the presence of the epoxide hydrolase inhibitor 1,1,1-trichloropropene oxide (TCPO), which prevents the further metabolism of phenytoin to an inert metabolite. In lymphocytes exposed to this system, cytotoxicity was measured by trypan blue dye exclusion and was expressed as the percentage increase in trypan blue-positive cells after the addition of TCPO. In the presence of TCPO, lymphocytes from 11 patients with halothane hepatitis exhibited an increase in cytotoxicity at 0.06 mM phenytoin that was eight times greater than the increase in healthy controls (54 +/- 10 per cent [mean +/- S.E.M.] vs. 7.1 +/- 2.2 per cent, P less than 0.0001). Patients with other liver diseases and persons recently exposed to halothane without adverse effects did not differ from healthy controls. In three patients with halothane hepatitis who were studied serially, the lymphocyte abnormality was still present after 13 months. Family studies revealed abnormal results on 10 cytotoxicity tests among 19 members of four families. We propose that there is a familial, constitutional susceptibility factor that predisposes persons to halothane hepatitis.

Adult↗
PubMed1997

Caffeine and halothane sensitivity of intracellular Ca2+ release is altered by 15 calcium release channel (ryanodine receptor) mutations associated with malignant hyperthermia and/or central core disease.

Malignant hyperthermia (MH) and central core disease (CCD) are autosomal dominant disorders of skeletal muscle in which a potentially fatal hypermetabolic crisis can be triggered by commonly used anesthetic agents. To date, 17 mutations in the human RYR1 gene encoding the Ca2+ release channel of skeletal muscle sarcoplasmic reticulum (the ryanodine receptor) have been associated with MH and/or CCD. Although many of these mutations have been linked to MH and/or CCD, with high lod (log of the odds favoring linkage versus nonlinkage) scores, others have been found in single, small families. Independent biochemical evidence for a causal role for these mutations in MH is available for only two mutants. Mutations corresponding to the human MH mutations were made in a full-length rabbit RYR1 cDNA, and wild type and mutant cDNAs were transfected into HEK-293 cells. After about 48 h, intact cells were loaded with the fluorescent Ca2+ indicator, fura-2, and intracellular Ca2+ release, induced by caffeine or halothane, was measured by photometry. Ca2+ release in cells expressing MH or CCD mutant ryanodine receptors was invariably significantly more sensitive to low concentrations of caffeine and halothane than Ca2+ release in cells expressing wild type receptors or receptors mutated in other regions of the molecule. Linear regression analysis showed that there is a strong correlation (r = 0.95, p < 0.001) between caffeine sensitivity of different RYR1 mutants measured by the cellular Ca2+ photometry assay and by the clinical in vitro caffeine halothane contracture test (IVCT). The correlation was weaker, however, for halothane (r = 0.49, p > 0.05). Abnormal sensitivity in the Ca2+ photometry assay provides supporting evidence for a causal role in MH for each of 15 single amino acid mutations in the ryanodine receptor. The study demonstrates the usefulness of the cellular Ca2+ photometry assay in the assessment of the sensitivity to caffeine and halothane of specific ryanodine receptor mutants.

Animals↗
PubMed1997

Physiologically based pharmacokinetic analysis of the concentration-dependent metabolism of halothane.

1. Previous studies with the halothane analogue and chlorofluorocarbon replacement 2,2-dichloro-1,1,1-trifluoroethane (HCFC-123) have shown that there are concentration-dependent, sex-specific differences in the rate of uptake during inhalation exposure in rat. Since it is well established that there are sex-specific differences in the control of enzyme activity in drug metabolism, male and female rats were exposed by inhalation to halothane concentrations ranging from 500 to 4000 ppm. 2. A physiologically based pharmacokinetic model describing the concentration-dependent reduction in uptake and metabolism of halothane in male and female rats was developed. The in vivo metabolic rate constants obtained were: for male rats, Km = 0.4 mg litre-1 (2.03 mumol litre-1) and Vmaxc = 9.2 mg kg1 h-1 (46.6 mumol kg1 h-1); for female rats, Km = 0.4 mg litre-1 (2.03 mumol litre-1) and Vmaxc = 10.2 mg kg-1 h-1 (51.7 mumol kg-1 h-1). 3. An equation describing the concentration-dependent decrease of hepatic metabolism of halothane successfully simulated the gas-uptake data. Simulation of cumulative urinary excretion of the major metabolite, trifluoroacetic acid, required introduction of a proportionality constant to limit the extent of reduction of halothane metabolism to 20% of the amount of enzyme activity. Good simulation of urinary excretion data was achieved, which was interpreted to indicate that, when only 20% of the enzyme is inactivated, the rate of enzyme resynthesis was adequate to replenish enzyme activity within 24 h. 4. A rapidly reversible, non-biological inactivation mechanism called "physical toxicity' is discussed as a possible explanation of concentration-dependent gas uptake.

Animals↗
PubMed1976

Errors in oxygen tension measurements caused by halothane.

Halothane, independent of oxygen tension, increased the signal of the gold/silver-silver chloride microelectrode. The output of microelectrodes at different oxygen tensions in the presence of increasing amounts of halothane has been measured. Halothane causes an increase in the electrode signal which is proportional to its concentration. This effect results from the polarographic reduction of halothane. It is concluded that the gold/silver-silver chloride microelectrode cannot be used to measure oxygen tension during halothane anaesthesia.

Anesthesia↗
PubMed1976

Haemodynamic interactions of high-dose propranolol pretreatment and anaesthesia in the dog. I: Halothane dose-response studies.

The effect of pretreatment for 3 weeks with propranolol 20 mg/kg/day on cardiovascular function during increasing depths of halothane anaesthesia (range 1.0-2.5% inspired halothane with IPPV and normocapnia) were studied in a group of seven closed-chest dogs which had been implanted previously with cardiovascular flow- and pressure-measuring instruments. The results were compared with those observed in a similar group of five untreated dogs. Propranolol pretreatment resulted in a small degree of additional cardiac depression at any inspired halothane concentration. The cardiac depressant effects of propranolol and halothane were found to be simply additive and therefore predictable. The presence of propranolol did not result in morbidity or mortality at any depth of halothane anaesthesia.

Animals↗
PubMed1976

Hepatic pathology and skin test reactions to trifluoro-acetylated autologous protein after repeated halothane anaesthesia in the guineapig.

The aetiology of the rare hepatic failure following halothane anaesthesia is not known. In an attempt to develop an experimental model, three groups of guineapigs were exposed to air or oxygen, a single 1% halothane administration, or five exposures of 1% halothane at weekly intervals. In an attempt to identify a hypersensitivity reaction, all animals were skin-tested with the common final metabolite of halothane, fluroxene and isoflurane: trifluoroacetic acid, prepared as a complex with autologous serum protein. Hepatic necrosis was found in all groups and did not correlate with positive skin reactions. There was an increase in fatty changes in the liver in animals anaesthetized with halothane.

Anesthesia, General↗
PubMed1978

Cardiac performance during prolonged halothane anaesthesia in the cat. Isolated heart muscle study.

The contractile response of papillary muscles, isolated from normal cats, to prolonged administration of halothane at minimum alveolar anaesthetic concentration (MAC) was studied. Average values of maximal velocity of shortening (Vmax) and maximal developed force (Fm) obtained in 12 muscles during the 1st, 2nd and 3rd hour of exposure to halothane anaesthesia were significantly less than those obtained during the control period and after recovery from halothane. There were no significant differences in values over a 3-h period. When post-extra-systolic potentiation was induced by paired electric stimulation, average values of Vmax and Fm increased significantly. We conclude that prolonged administration of halothane at a constant concentration resulted in a sustained depression of myocardial contractility without tissue tolerance. The myocardium depressed by halothane, however, still retains the ability to respond to additional inotropic stimulation.

Anesthesia, General↗