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PubMed2006

Propofol, more than halothane, depresses electroencephalographic activation resulting from electrical stimulation in reticular formation.

BACKGROUND: Halothane and propofol depress the central nervous system, and this is partly manifested by a decrease in electroencephalographic (EEG) activity. Little work has been performed to determine the differences between these anesthetics with regard to their effects on evoked EEG activity. We examined the effects of halothane and propofol on EEG responses to electrical stimulation of the reticular formation. METHODS: Rats (n= 12) were anesthetized with either halothane or propofol, and EEG responses were recorded before and after electrical stimulation of the reticular formation. Two anesthetic concentrations were used (0.8 and 1.2 times the amount needed to prevent gross, purposeful movement in response to supramaximal noxious stimulation), and both anesthetics were studied in each rat using a cross-over design. RESULTS: Electrical stimulation in the reticular formation increased the spectral edge (SEF) and median edge (MEF) frequencies by approximately 1-2 Hz during halothane anesthesia at low and high concentrations. During propofol anesthesia, MEF increased at the low propofol infusion rate, but SEF was unaffected. At the high propofol infusion rate, SEF and MEF decreased following electrical stimulation in the reticular formation. CONCLUSIONS: At immobilizing concentrations, propofol produces a larger decrease than halothane in EEG responses to reticular formation stimulation, consistent with propofol having a more profound depressant effect on cortical and subcortical structures.

Anesthetics, Inhalation↗
PubMed1992

Molecular mimicry of trifluoroacetylated human liver protein adducts by constitutive proteins and immunochemical evidence for its impairment in halothane hepatitis.

A monospecific antibody (anti-CF3CO antibody) was obtained by affinity chromatography on a N epsilon-trifluoroacetyl-L-lysine (CF3CO-Lys) matrix of a rabbit polyclonal antiserum, directed against trifluoroacetylated protein adducts (CF3CO-proteins). The anti-CF3CO antibody recognized distinct CF3CO-proteins on immunoblots of a liver biopsy obtained from a human individual 10 h after halothane anaesthesia. Cross-reactive proteins of 52 kDa and 64 kDa were recognized on immunoblots of livers obtained from human individuals not exposed to halothane. Recognition of both CF3CO-proteins and the 52-kDa and 64-kDa cross-reactive proteins was abolished in the presence of 1 mM CF3CO-Lys. Anti-CF3CO antibody, affinity-adsorbed to the 52-kDa or the 64-kDa cross-reactive proteins of human liver, recognized the majority of target CF3CO-proteins on immunoblots of the human liver biopsy of an individual exposed to halothane. Liver biopsies of 5 out of 7 (71%) patients with halothane hepatitis exhibited an absence or low amounts of immunorecognizable 52-kDa and/or 64-kDa cross-reactive proteins. In contrast, of 22 control human individuals tested, all liver tissue samples were positive for the 52-kDa and/or the 64-kDa cross-reactive proteins. These data indicate that epitopes on the cross-reactive proteins of 52 kDa and 64 kDa of human liver bear strong immunochemical resemblance to epitopes on human liver CF3CO-proteins. Low-level expression of the cross-reactive proteins of 52 kDa and 64 kDa is discussed as one possible factor in human susceptibility to halothane hepatitis.

Adult↗
PubMed1994

Leukotriene B4 formation upon halothane-induced lipid peroxidation in liver membrane fractions under low O2 concentrations in vitro.

Lipid peroxidation was induced in rat liver membrane fractions in vitro upon NADPH-dependent metabolic activation of the anesthetic agent halothane at low O2 concentrations. Halothane-induced lipid peroxidation was dependent on time, concentration of halothane, and the calculated O2 concentrations present in the system. Lipid peroxidation was inducible at increasing O2 concentrations up to 12 microM, decreased at higher O2 concentrations up to 48 microM, and was not detectable at normoxic conditions. Leukotriene B4 (LTB4) was identified as a product arising upon lipid peroxidation by reverse-phase high-pressure liquid chromatography combined with a radioimmunoassay. LTB4 formation was maximal under conditions of maximal lipid peroxidation at a calculated O2 concentration of 12 microM. Even at high concentrations, the 5-lipoxygenase inhibitors MK886 (10 microM), ZD2138 (20 microM), and ZM230487 (20 microM) were not inhibitory in halothane-induced lipid peroxidation nor in the associated formation of LTB4. Synthetic LTB4 was transformed into its 20-hydroxy derivative by omega-oxidation in an O2-concentration-dependent manner, being considerably reduced at the low O2 concentrations that maximally promoted lipid peroxidation. The collective evidence of these data raises the possibility that exposure to halothane might lead to peroxidation-associated net synthesis of LTB4 through 5-lipoxygenase-independent escape routes in liver tissue under physiologically or pathophysiologically low O2 concentrations.

Aerobiosis↗
PubMed2005

Effects of tail fat on halothane biotransformation in fat-tailed sheep.

1. The aim of the present study was to evaluate the effects of tail fat on halothane biotransformation following similar anaesthetic exposure in intact sheep and sheep with a ligated median sacral artery. 2. A prospective randomized experimental study was performed using 12 healthy, 10-12-month-old female sheep. 3. Sheep were randomly divided into two groups of six animals each and were anaesthetized twice at 2 weekly intervals. After mask induction with halothane in 100% oxygen, sheep were intubated and anaesthesia was maintained for 3 h using a rebreathing system. Serum fluoride concentration (SFC) was measured at 0, 1, 3, 6, 12, 24, 48 and 72 h following the induction of anaesthesia. Serum biochemistry was also evaluated at baseline and 72 h after anaesthesia. Induction and extubation times and time to sternal recumbency were also recorded during anaesthetic induction and recovery. Prior to the second anaesthesia (2 weeks later), the median sacral artery (MSA) was ligated under epidural anaesthesia in the experimental group. Sheep in the control group underwent sham operation. All sheep were anaesthetized as before. 4. Following the first halothane anaesthesia, SFC was significantly increased from 3 to 48 h compared with baseline. In the second stage of the experiment, the increases in SFC in the control group were similar to those seen in the first stage of the experiment. However, in MSA-ligated sheep, the increases in SFC were only significant between 3 and 12 h compared with baseline. The SFC was significantly higher in intact sheep from 3 to 72 h compared with the MSA-ligated group. Extubation and sternal recumbency times were significantly longer in intact sheep. 5. Ligation of the MSA in fat-tailed sheep induced a significant reduction in SFC, suggesting that the presence of tail fat substantially affects halothane metabolism during the peri-anaesthetic period in sheep. The greater extent of halothane biotransformation may be clinically important in, otherwise normal, obese patients.

Administration, Inhalation↗
PubMed1994

The effect of halothane on neonatal ciliary beat frequency.

The effect of a commonly used anaesthetic agent, halothane, on neonatal cilial function was determined. A nasal cilial sample was taken from 13 healthy, term, newborn infants. For 1 h, half of each sample was exposed to halothane and half to air. Cilial function was assessed by measuring beat frequency with a modified light transmission method. Cilial beat frequency was significantly slower in the cilia exposed to halothane, 9(s.d. 2.5)Hz, than to air, 12.9(s.d. 1.5)Hz. Decreased mucociliary clearance following halothane anaesthesia is due, at least in part, to a directly depressant effect of halothane on ciliated cells.

Air↗
PubMed1989

Risk factors for halothane hepatitis.

Helothane hepatitis is a rare but sometimes fatal complication of halothane anaesthesia. Examination of case reports has pointed to a number of risk factors. Studies in animals and humans in the laboratory have provided evidence of a complex multifactorial basis for halothane hepatotoxicity, with the following factors playing a part: genetic predisposition; metabolism of halothane; repeated halothane anaesthetics; female sex; age of patient; intrahepatic hypoxia; and enzyme induction. Immunologic changes can be detected in a high percentage of cases of halothane hepatitis; however, studies establishing a cause-effect relationship are not available to determine if these changes cause, or result from, hepatic damage.

Anesthesia↗
PubMedDate not supplied

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↗
PubMedDate not supplied

Anesthesia in sheep with propofol or with xylazine-ketamine followed by halothane.

OBJECTIVE: This study evaluates the clinical usefulness and anesthetic effect of propofol, and compares these effects with those of xylazine-ketamine-halothane anesthesia in sheep. STUDY DESIGN: Prospective, randomized, clinical trial. ANIMALS OR SAMPLE POPULATION: Fourteen healthy adult male sheep. METHODS: Sheep were randomly assigned to two different drug regimens: (1) Bolus injection of propofol (3 mg/kg, intravenously [i.v.]) followed by continuous intravenous infusion and (2) xylazine (0.11 mg/kg, i.v.) and ketamine (2.2 mg/kg, i.v.) for induction followed by halothane anesthesia. Heart rate, respiratory rate, and arterial blood pressures were monitored during anesthesia. Venous blood samples were collected for blood gas analysis. Quality of induction and recovery were also recorded. RESULTS: The average dose of propofol used to induce and maintain anesthesia was 6.63 +/- 2.06 mg/kg and 29.3 +/- 11.7 mg/kg/hr (0.49 +/- 0.20 mg/kg/min), respectively. The duration of propofol anesthesia was 45.3 +/- 13.2 minutes and recovery to standing occurred in 14.7 +/- 5.7 minutes. Sheep receiving xylazine-ketamine-halothane were anesthetized for 35.9 +/- 4.0 minutes and recovery to standing occurred within 28.5 +/- 7.5 minutes. Sheep anesthetized with propofol had a significantly higher heart rate, diastolic blood pressure and Pvo2, and a lower Pvco2 at 30 minutes and lower BE at 15 and 30 minutes than sheep anesthetized with xylazine-ketamine-halothane. CONCLUSIONS: Propofol anesthesia was characterized by a smooth induction, effective surgical anesthesia and rapid recovery which was comparable to anesthesia with xylazine-ketamine-halothane. CLINICAL RELEVANCE: Propofol may be indicated in situations when it is desirable to maintain anesthesia with an intravenous infusion followed by a rapid recovery in healthy sheep.

Anesthesia, Inhalation↗
PubMed1988

Enhanced in vivo-lipid peroxidation associated with halothane hepatotoxicity in rats.

To study the role of lipid peroxidation in halothane-induced hepatic damage, ethane exhalation by rats exposed to 1% halothane for 1 hour was determined under normoxic (21% O2) and hypoxic (6% O2) conditions. The effects of microsomal enzyme induction by phenobarbital and/or glutathione depletion on this parameter of in vivo lipid peroxidation were studied. To assess the degree of liver damage, serum activities of liver specific enzymes (glutamate-pyruvate-transaminase, GPT, and sorbitol dehydrogenase, SDH) were measured 3 hrs after the end of exposure. Besides, liver content of thiobarbituric acid-reactive material was estimated as a further parameter of lipid peroxidation. Enhanced rates of lipid peroxidation over basal levels were only seen under conditions leading to hepatic damage, i.e. phenobarbital induction and hypoxia. The highest rate of lipid peroxidation was observed after depletion of hepatic glutathione in addition to microsomal enzyme induction and hypoxia. Deferrioxamine, diethyldithiocarbamate and (+)-catechin inhibited in vivo lipid peroxidation, but only (+)-catechin suppressed halothane-hepatoxicity. These results indicate that halothane-induced hepatic damage is associated with an enhanced rate of lipid peroxidation, but this might not be the only mechanism of halothane toxicity.

Animals↗
PubMed1988

Halothane induced hepatic necrosis in rats: the role of in vivo lipid peroxidation.

Hepatic damage was induced in phenobarbitone pretreated male Fischer 344 rats by the administration of 1% halothane in 14% oxygen for either 1 or 2 hours. Ethane production during the exposure period was not significantly different between the halothane and non-halothane exposed groups. Animals were sacrificed 1, 2, 6 and 24 hrs from commencement of anaesthesia and the hepatic microsomal fraction analyzed for diene conjugates, lipid hydroperoxides, total lipid content and fatty acid composition. Animals exposed to halothane and sacrificed at 2 and 24 hrs had significantly elevated levels of diene conjugates (P less than 0.05), while lipid hydroperoxide concentration and serum alanine aminotransferase increased in only those animals sacrificed at 24 hrs. Alterations in total lipid content and hepatic microsomal fatty acid composition were not observed in animals sacrificed after 1 and 2 hrs. A significant reduction in total lipid and arachidonic acid content occurred only in those animals sacrificed 24 hrs after exposure, however a concomitant increase in the saturated fatty acid fraction was not observed. It is proposed that alterations in fatty acid composition in vivo and evidence of lipid peroxidation occur as a result of cell death rather than an initiating event in halothane induced hepatic necrosis in rats.

Alanine Transaminase↗
PubMed2005

Effects of adenosine agonist R-phenylisopropyl-adenosine on halothane anesthesia and antinociception in rats.

AIM: To investigate the antinociceptive effect of adenosine agonist R-phenylisopropyl-adenosine (R-PIA) given to conscious rats by intracerebroventricular (ICV) and intrathecal (IT), and identify the effect of R-PIA on minimum alveolar concentration (MAC) of halothane with pretreatment of A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) or K+ channel blocker 4-aminopyridine (4-AP). METHODS: Sprague-Dawley rats were implanted with 24-gauge stainless steel guide cannula using stereotaxic apparatus and ICV method, and an IT catheter (PE-10, 8.5 cm) was inserted into the lumbar subarachnoid space, while the rats were under pentobarbital anesthesia. After one week of recovery from surgery, rats were randomly assigned to one of the following protocols: MAC of halothane, or tail-flick latency. All measurements were performed after R-PIA (0.8-2.0 microg) microinjection into ICV and IT with or without pretreatment of DPCPX or 4-AP. RESULTS: Microinjection of adenosine agonist R-PIA in doses of 0.8-2.0 microg into ICV and IT produced a significant dose- and time-dependent antinociceptive action as reflected by increasing latency times and ICV administration of adenosine agonist R-PIA (0.8 microg) reducing halothane anesthetic requirements (by 29%). The antinociception and reducing halothane requirements effected by adenosine agonist R-PIA was abolished by DPCPX and 4-AP. CONCLUSION: ICV and IT administration of adenosine agonist R-PIA produced an antinociceptive effect in a dose-dependent manner and decreased halothane MAC with painful stimulation through activation of A1 receptor subtype, and the underlying mechanism involves K+ channel activation.

4-Aminopyridine↗
PubMed1985

Effects of halothane on the transducer and potential activated currents of the crustacean stretch receptor.

Halothane was applied to the stretch receptor neuron of the crayfish (Astacus astacus) and the effects on the transducer properties and the potential activated currents were studied with potential clamp technique using two microelectrodes. Exposure to halothane reduced the frequency of action potentials during stretch. This was shown to be due to effects both on the action potential generating currents and the transducer current. Halothane partially blocked the TTX sensitive fast inward current in a dose-dependent manner (Apparent KD = 3 mM). Halothane also reduced the outward current produced by a positive potential step. Both the fast and the slow component were affected, although the fast outward current seemed to be most sensitive. There was little or no change in the currents resulting from negative potential steps. The peak of the receptor potential and the receptor current were very little affected by halothane. The amplitude of the static phase of the receptor potential was reduced to a greater degree than the static phase of the receptor current (cells treated with TTX). A change in reversal potential of about--13 mV was observed for the peak and the static phase of the receptor current in four cells indicating an increased cord conductance for the transducer channel.

Action Potentials↗
PubMed1995

The haemodynamic effects of milrinone HCl in halothane anaesthetised horses.

The haemodynamic effects of milrinone hydrochloride were determined in halothane-anaesthetised horses. Six healthy adult horses were anaesthetised with guaifenesin and thiamylal and maintained with halothane in oxygen (end-tidal halothane concentration of 1.15%). Baseline haemodynamic data were recorded after a 45 min stabilisation period. All 6 horses received a single loading dose of milrinone HCl, 0.2 microgram/kg i.v., followed by progressively increasing infusions of 2.5, 5, 10 and 20 micrograms/kg bwt/min. Each infusion lasted for 15 min and produced dose related increases in heart rate, mean arterial blood pressure, cardiac output, maximum rate of increase and decrease of left ventricular pressure (+/- dP/dtmax) and ejection fraction in halothane anesthetised horses. Median artery blood flow increased following milrinone administration. Right atrial and pulmonary artery pressures, systemic vascular resistance and left ventricular end-diastolic and end-systolic volumes decreased. Most haemodynamic changes were sustained throughout the infusion period and for 30 min following the termination of milrinone infusion. Systemic vascular resistance was increased above baseline values at 30 min following the termination of milrinone infusion. No adverse side effects were observed during this study although a milrinone infusion rate of 20 micrograms/kg bwt/min increased heart rate to values greater than 50 beats/min. The results of this study suggest that milrinone produces beneficial haemodynamic effects in halothane anaesthetised horses and is potentially useful in the treatment of patients with a reduced cardiac output.

Anesthetics, Inhalation↗
PubMed1966

The effects of cyclopropane, halothane and ether on central baroreceptor pathways.

1. The reductions in arterial pressure and preganglionic sympathetic activity evoked by aortic nerve stimulation in the rabbit were studied before and during administration of constant inspired concentrations of the inhalation anaesthetics cyclopropane, halothane, and ether. The background anaesthetic was pentobarbitone, gallamine triethiodide was given, and pulmonary ventilation was with 100% oxygen.2. During light pentobarbitone anaesthesia, aortic nerve stimulation usually induced similar reductions in arterial pressure and preganglionic discharge, expressed as the maximum percentage reduction from prestimulation levels. There were two components in the sympathetic responses, attributable to A and C fibre excitation in the aortic nerve, which was also shown to contain a third fibre group with properties similar to those of B fibres.3. The arterial pressure, heart rate, and preganglionic sympathetic responses to aortic nerve stimulation were rapidly and profoundly inhibited by 50% cyclopropane, which also produced arterial hypertension.4. Halothane (3%) significantly inhibited the depressor responses, but even in the presence of severe hypotension the arterial pressure could usually be further reduced by aortic nerve stimulation. The inhibitory effects of 2% halothane were slow in onset and not pronounced. In the concentrations used, these actions of halothane were significantly less than those of cyclopropane.5. The inhibitory effects of ether on the depressor responses were roughly intermediate between those of cyclopropane and halothane; complete suppression of the responses occurred with high ether concentrations, which were also liable to cause circulatory collapse.6. It is concluded that the three anaesthetics significantly inhibit impulse transmission through central baroreceptor pathways; the implications of the findings are discussed in relation to the different circulatory actions of these anaesthetics.

Action Potentials↗
PubMed1987

Halothane hepatitis in children.

It is often stated that halothane hepatitis in children is nonexistent or extremely rare. This syndrome occurred in seven children aged between 11 months and 15 years, one of whom, a 3 1/2 year old boy, died with fulminant hepatic failure. All the children had received multiple halothane anaesthetics (range 2-6, median 3). In all cases other causes of liver diseases were excluded, and in all but one the diagnosis was confirmed serologically by antibodies to halothane altered liver cell membrane antigens. These findings suggest that halothane hepatitis occurs in children, and the risk of halothane hepatitis should therefore be considered when choosing which agents to use in children who require multiple anaesthetics.

Adolescent↗
PubMed1990

Halothane-dependent release of intracellular Ca2+ in blood cells in malignant hyperthermia.

The concentration of ionized cytosolic calcium [( Ca2+]i) was determined in peripheral blood mononuclear cells from normal and malignant hyperthermia (MH)-susceptible humans and pigs, using the fluorescent Ca2+ indicator indo-1. [Ca2+]i was slightly but significantly elevated in cells from MH human cells relative to normal cells (198 +/- 18 nM, n = 15, and 146 +/- 14 nM, n = 11, respectively, P less than 0.05). Anesthetic concentrations of halothane in the cell suspension resulted in a rapid increase in [Ca2+]i in cells from both normal and MH humans or pigs. The increases (delta) were more pronounced in cells from MH subjects than from normal individuals (delta at 5.7 mM halothane: 245 +/- 53 vs. 57 +/- 11 nM, respectively) and from MH than from normal pigs (delta of 241 +/- 63 vs. 53 +/- 27 nM, respectively). Removal of extracellular Ca2+ obliterated the delta[Ca2+]i caused by halothane in cells from normal humans or pigs but only decreased by about half the delta[Ca2+]i in cells from MH humans or pigs. In 1,2-bis-(aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA)-loaded cells, in the absence of extracellular Ca2+, halothane failed to increase [Ca2+]i. This suggests that buffering Cai2+ with BAPTA precludes detection of release of Ca2+ from intracellular stores, explaining the previous observations made with quin2, a highly chelating Ca2+ indicator. It is concluded that clinical concentrations of halothane allow influx of Ca2+ in cells from both normal and MH-susceptible individuals but release Ca2+ from intracellular stores selectively in cells from the latter group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effects of halothane, enflurane, and isoflurane on skinned rat myocardium activated by Ca2+.

The effects of halothane (1.9 mM, 9.4 mM), enflurane (3.3 mM, 16.5 mM), and isoflurane (1.6 mM, 8.1 mM) on maximal Ca(2+)-activated force and Ca2+ sensitivity were studied in rat myocardial preparations rendered permeable by various methods. In preparations permeabilized either by mild homogenization or by saponin (50 micrograms/ml, 30 min), further disruption of the sarcolemma with 2% Triton X-100 resulted in increased maximal force and Ca2+ sensitivity. When membranes were mechanically disrupted or saponized, each vapor agent caused the myocardium to be more sensitive to Ca2+. In these preparations, maximal force was decreased by halothane but was not affected by enflurane or isoflurane. With cellular membranes completely disrupted by Triton, the previously observed increase in Ca2+ sensitivity caused by enflurane was reduced, whereas that caused by halothane and isoflurane was abolished and maximal force was decreased by halothane and isoflurane but was not affected by enflurane. These results indicate that 1) components associated with the cellular membrane systems normally modulate force in mammalian myocardium, and 2) halothane, enflurane, and isoflurane have complex effects on these components. These results therefore can explain some of the differences in inotropic effects that these agents exert on mammalian myocardium.

Animals↗
PubMed1998

Effects of halothane on [Ca2+]i transient, SR Ca2+ content, and force in intact rat heart trabeculae.

The goal of this study was to test whether the well-known cardiodepressant effect of halothane is caused mainly by depression of the transient increase in intracellular Ca2+ concentration ([Ca2+]i) during a twitch. Intact rat ventricular trabeculae, paced at 0.5 Hz and 30 degrees C with a bathing extracellular Ca2+ concentration ([Ca2+]o) of 2 mM, were used. The [Ca2+]i was monitored with the use of fura 2 injected into the myoplasm. The sarcoplasmic reticulum (SR) Ca2+ content was estimated with the use of rapid cooling (RC)-induced contracture force and Ca2+ release. The relationship of the peak [Ca2+]i transient versus peak twitch force obtained with halothane is intermediate between those obtained with lowered [Ca2+]o and varying doses of 2,3-butanedione monoxime. The data indicate that the negative inotropic action of halothane at low (0.18 mM) dose is mainly achieved by reduction in the Ca2+ sensitivity of the contractile apparatus, whereas, at high dose (0.55 mM), halothane acts both by reducing the [Ca2+]i transient and the Ca2+ sensitivity of the contractile system. At moderate (0.37 mM) dose, the effects were midway between low and high doses. With the use of RC contracture force alone, the reduction of SR Ca2+ content caused by halothane is overestimated.

Animals↗