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PubMedDate not supplied

Neonatal acid-base status following general anesthesia for emergency abdominal delivery with halothane or isoflurane.

STUDY OBJECTIVE: To determine whether halothane or isoflurane as anesthesia for emergency abdominal delivery is associated with better fetal acid-base parameters. DESIGN: Randomized study. SETTING: Inpatient Level III perinatal referral center in a university hospital. PATIENTS: Sixty-six gravidas undergoing emergency abdominal delivery under general anesthesia for fetal distress. INTERVENTIONS: Randomization to receive halothane or isoflurane at 0.7 minimum alveolar concentration as part of a standard anesthetic technique. MEASUREMENTS AND MAIN RESULTS: Umbilical artery and vein blood gases were obtained and compared for hydrogen ion concentration, partial pressure of carbon dioxide, partial pressure of oxygen, and base deficit. There were no significant differences between the isoflurane and halothane groups. CONCLUSIONS: There is no difference in the frequency or severity of acidosis associated with isoflurane or halothane when used for general anesthesia for emergency abdominal delivery of a distressed fetus.

Acid-Base Equilibrium↗
PubMed1995

Comparison of sevoflurane and halothane anesthesia in children undergoing outpatient ear, nose, and throat surgery.

STUDY OBJECTIVE: To compare the induction, maintenance, and recovery characteristics of sevoflurane and halothane in pediatric ambulatory patients undergoing adenoidectomy with or without myringotomies (BMTs). To compare the hemodynamic effects of the two drugs. DESIGN: Open, randomized study. SETTING: University-affiliated pediatric hospital. PATIENTS: 39 ASA physical status I children aged 12 months to 12 years undergoing adenoidectomies with or without BMTs. INTERVENTIONS: Patients were randomized to receive sevoflurane or halothane in 60% nitrous oxide (N2O) for induction and maintenance of anesthesia. All patients received midazolam 0.5 mg/kg orally as premedication, as well as fentanyl 1 mcg/kg intravenously (i.v.) immediately following induction. Tracheal intubation was facilitated with mivacurium 0.2 mg/kg i.v. Anesthesia was maintained with an end-tidal concentration corresponding to 1 minimum alveolar concentration (MAC) of each drug until the end of surgery, at which time all anesthetic gases were discontinued simultaneously. Emergence (extubation), recovery (Steward score = 6), and discharge times were compared among patients in both groups. Heart rate (HR) and mean arterial pressure were compared at predetermined intervals. Additional fentanyl was administered after full recovery was documented for an objective pain score of at least 6. MEASUREMENTS AND MAIN RESULTS: Emergence from anesthesia was significantly faster (7.11 +/- 3.05 minutes vs. 9.58 +/- 5.12 minutes) and recovery (19.89 +/- 10.07 minutes vs. 31.08 +/- 9.81 minutes) more rapid in the sevoflurane group. However, there was no difference in the time to meet home discharge criteria (184 +/- 49 minutes vs. 189 +/- 48 minutes). HR was consistently maintained at or above baseline in the sevoflurane group. Blood pressure was significantly more depressed after fentanyl administration in the halothane group. There were no significant differences in the incidence of postoperative vomiting between the two groups. CONCLUSION: Sevoflurane provides a faster anesthetic emergence and recovery than halothane in premedicated patients but it does not expedite meeting current home discharge criteria.

Adenoidectomy↗
PubMed1996

A comparison of sevoflurane with halothane in outpatient adenotomy in children with mild upper respiratory tract infections.

STUDY OBJECTIVE: To investigate the efficacy and safety of sevoflurane compared with halothane in pediatric outpatient ear-nose-throat (ENT) surgery during the induction, maintenance, emergence, and recovery of anesthesia. DESIGN: Prospective, randomized, comparative, open-label study. SETTING: ENT operating room and postoperative recovery room at a university medical center. PATIENTS: 41 ASA status I and II children between the ages of 2 to 10 years, with mild upper respiratory tract infection (URI). INTERVENTIONS: Induction and maintenance of anesthesia with either sevoflurane or halothane for outpatient adenotomy, otomicroscopy, and myringotomy. MEASUREMENTS AND MAIN RESULTS: Induction (means +/- SEM) was significantly shorter in the sevoflurane group (2.6 +/- 0.2 minutes) than in the halothane group (3.2 +/- 0.2 minutes). There was no difference between the two groups with regard to complications that occurred during the induction and maintenance period. The time to emergence and recovery was significantly shorter with sevoflurane than with halothane (means +/- SEM; time to extubation 9.9 +/- 0.98 minutes vs. 13.4 +/- 1.06 minutes, time to eye opening 12.9 +/- 1.6 minutes vs. 24.5 +/- 1.8 minutes, command response time 20.7 +/- 2.5 minutes vs. 36.4 +/- 2.8 minutes). No difference in the incidence of complications during emergence and recovery was found. Evaluation of recovery as assessed by a modified Aldrete score showed that children who had received sevoflurane reached higher scores in the first 30 minutes following the discontinuation of the anesthetic. The Pain/Discomfort Scale demonstrated a difference in the sevoflurane group, with more children being agitated and restless. CONCLUSION: Sevoflurane provides a safe and rapid anesthetic induction with no differences in complications during the induction, maintenance, and emergence period. With sevoflurane, the time of emergence and recovery was significantly shorter. The characteristics of sevoflurane as evaluated in the present study make it a suitable anesthetic in pediatric outpatient surgery even in the presence of mild URI.

Adenoids↗
PubMed1994

Effects of sevoflurane, isoflurane, enflurane, and halothane on left ventricular diastolic performance in dogs.

The effects of volatile anesthetics on active (ventricular relaxation) and passive (chamber stiffness) indices of diastolic function and on left ventricular filling rates in dogs were studied to determine how these agents affect left ventricular diastolic performance. Thirty-five mongrel dogs were randomly assigned to receive sevoflurane, isoflurane, enflurane, or halothane. Left ventricular pressure waveforms, phonocardiograms, and echocardiograms were recorded after administering the anesthetics at concentrations of 0% (control), 1%, 2%, and 3%. Ventricular relaxation was defined as the time constant of the decline in left ventricular pressure. Chamber stiffness was derived from the ventricular pressure-volume relationship during passive filling. Rapid filling rate, slow filling rate, and atrial filling rate were obtained from echocardiograms and phonocardiograms. No change in the time constant or in chamber stiffness was observed at any concentration of sevoflurane or isoflurane. However, the highest studied concentration of enflurane and halothane produced a significant increase in the time constant and in chamber stiffness. Rapid filling rate as well as atrial filling rate decreased significantly with the volatile anesthetics, especially with enflurane and halothane. Sevoflurane and isoflurane did not alter ventricular relaxation or chamber stiffness, but did affect diastolic function as manifested by their alteration of filling rates. In contrast, enflurane and halothane each prolonged ventricular relaxation and increased chamber stiffness. With the administration of the volatile anesthetics, the rapid filling rate decreased with the deterioration of diastolic function; in addition, atrial filling rates decreased and did not compensate for the reduction in early ventricular filling.

Anesthetics, Inhalation↗
PubMed2007

Detrimental effects of halothane narcosis on damage after endothelin-1-induced MCAO.

The influence of anaesthesia in experimental stroke research is controversial. We addressed this problem using the model of endothelin-1-induced occlusion of the middle cerebral artery (eMCAO). This model provided the opportunity to compare the infarct volumes of rats which were under halothane anaesthesia during eMCAO induction with the lesions of rats which were without anaesthesia during eMCAO. All animals were implanted with guide cannulae which allowed the induction of ischaemia in freely moving animals. For comparison, one group of animals was exposed to halothane during the induction of ischaemia. Seven days after eMCAO, the average infarct volume of halothane-anaesthetised rats was significantly larger than the lesion in freely moving animals. This difference was mainly due to increased cortical damage, whereas the striatum was much less influenced. The cortical infarct volume 21 days after induction of eMCAO under anaesthesia was significantly reduced compared to the infarct volume 7 days after eMCAO under anaesthesia. Our results indicate that halothane anaesthesia during eMCAO can cause a transient cortical increase in ischaemic infarct volume. The influence of volatile anaesthetics on ischaemic pathophysiology should be taken into consideration when preclinically testing potential neuroprotective drugs for clinical applications.

Anesthetics, Inhalation↗
PubMed2007

Comparison of functional activity in the rat cervical spinal cord during alpha-chloralose and halothane anesthesia.

Alpha-chloralose is commonly used during animal fMRI studies for anesthesia, however, recovery of animals is difficult, limiting experimental design. The use of a less invasive anesthetic would enable chronic experiments. The present study compares functional activity in the spinal cord of the alpha-chloralose and halothane-anesthetized rat. Functional MRI of the rat cervical spinal cord was performed on 6 alpha-chloralose and 6 halothane-anesthetized rats in a Bruker 7 T MR system during electrical stimulation of the right forepaw. Following imaging, four animals from each group were perfused and spinal cords removed for immunohistochemical analysis. Areas of c-fos expression were identified with immunofluorescent labeling to confirm the presence of neuronal activity. Functional activity and c-fos expression were observed predominantly between the fifth and seventh cervical spinal cord segments. Areas of fMRI activation in the spinal cord correspond well with spinal cord physiology. Areas of c-fos expression confirmed that neuronal activity was present in the regions of fMRI activity. The regions and amount of fMRI activity observed were similar for both anesthetics. Functional magnetic resonance imaging of the spinal cord can be achieved using both alpha-chloralose and halothane anesthesia in rats. We therefore suggest that halothane may be used as an anesthetic agent for chronic fMRI studies of the spinal cord.

Anesthetics, Inhalation↗
PubMed1977

Oxygen consumption during surface-induced deep hypothermia under halothane anesthesia.

The effect of halothane-100% oxygen anesthesia on oxygen consumption was studied in 10 dogs subjected to surface-induced deep hypothermia with 30 minutes of circulatory arrest. The results were compared with previous oxygen consumtion data under ether-100% oxygen anesthesia. Low cardiac output, especially during the rewarming period, low PaO2, and a large arteriovenous oxygen difference during rewarming were significantly different in the halothane group, despite identical oxygen consumption in both groups. These differences could not elucidate the exact cause of postoperative motor disturbances associated with 30 minutes of circulatory arrest in the halothane group. The possibility that there was higher oxygen consumption under halothane anesthesia is discussed.

Anesthesia↗
PubMed1976

Effects of morphine and halothane anesthesia on coronary blood flow.

This study was undertaken to determine the relative effects of morphine and halothane anesthesia on coronary blood flow. Right heart bypass was instituted in 20 dogs by draining the vena cava blood into a cardiotomy reservoir and returning it to the main pulmonary artery. Coronary sinus drainage was measured by a right ventricular cannula. Group I (10 dogs) was sequentially given 0.5, 1, 1.5, 2.0, and 2.5% halothane. Group II (10 dogs) was given 1, 2, 3, 4, and 5 mg per kilogram of morphine intravenously. Arterial pressure, coronary sinus blood flow, cardiac output, arterial pH, PCO2, and PO2 were determined and repeated at each dose level of anesthesia and compared to the control values. Morphine significantly increased coronary flow at 3, 4, and 5 mg/kg without pressure adjustment and at 2 mg/kg after pressure adjustment. Coronary flow with halothane was unchanged from control values except for a decrease at 2.5%. Coronary flow was significantly greater with 3, 4, and 5 mg/kg of morphine than with 1.0 and 1.5% halothane.

Anesthesia, Inhalation↗
PubMed1986

Involvement of long-chain acyl CoA in the antagonistic effects of halothane and L-carnitine on mitochondrial energy-linked processes.

Incubation of rat liver mitochondria in the presence of halothane induced a consistent impairment of mitochondrial oxidative phosphorylation without significantly affecting the steady-state of transmembrane electrical potential. These alterations of mitochondrial energy-linked processes were associated with a consistent accumulation of long-chain acyl CoA. Addition of L-carnitine partially prevented the effects of halothane on oxidative phosphorylation and completely abolished the halothane-induced long-chain acyl CoA accumulation. The possibility is discussed that the damaging action of halothane on mitochondrial functions might be partially ascribed to the noxious action of the excess of long-chain acyl CoA induced the anesthetic.

Acyl Coenzyme A↗
PubMed1995

Reductive activation of halothane by human haemoglobin results in the modification of the prosthetic haem.

The metabolic activation of halothane by human haemoglobin (Hb) under reducing conditions in vitro is reported. Absolute spectra of sodium dithionite-reduced Hb, recorded during its anaerobic incubation in the presence of the substrate, showed decreasing concentrations of reduced Hb (Hb2+) with time. The loss of Hb2+ was accompanied, although only to some extent, by a concurrent oxidation to methaemoglobin (Hb3+), suggesting that electron transfer from Hb to the substrate had occurred. Reductive halothane metabolism was observed under these conditions as indicated by a dose-dependent inorganic fluoride (F-) production, which was, however, lower than that observed with heated Hb or a water soluble haem preparation (methaemalbumin). A rapid, partial loss of Hb was found upon addition of the substrate to the incubation mixture, as indicated by a decrease of the typical peak at 418 nm in the absolute spectra recorded in the presence of carbon monoxide (CO). This effect was associated with a loss of the Hb prosthetic group, haem, as shown by a decrease of the pyridine-haemochromogen reaction. Both effects were time and dose dependent. The inhibition of the Hb inactivation reaction by adding exogenous CO or the spin trapping agent N-t-butyl-alpha-phenylnitrone (PBN) to the incubation mixture beforehand indicated that (a) a reduced and free haem iron is required by Hb to activate halothane, and (b) the formation of free radical reactive metabolites of halothane is likely to be responsible for Hb inactivation. The mechanism of the reaction may involve the attack of these metabolites on the haem group of Hb, as indicated by the detection, with a reverse-phase ion-pairing HPLC system, of two Hb-derived products showing a typical haem-like absorption spectrum. The present results resemble those obtained recently with carbon tetrachloride (Ferrara et al., Alternatives to Laboratory Animals 21: 57-64, 1993) and suggest a common mechanism of activation of the two polyhalogenated alkanes by Hb.

Biotransformation↗
PubMed2000

Distribution of halothane in a dipalmitoylphosphatidylcholine bilayer from molecular dynamics calculations.

We report a 2-ns constant pressure molecular dynamics simulation of halothane, at a mol fraction of 50%, in the hydrated liquid crystal bilayer phase of dipalmitoylphosphatidylcholine. Halothane molecules are found to preferentially segregate to the upper part of the lipid acyl chains, with a maximum probability near the C(5) methylene groups. However, a finite probability is also observed along the tail region and across the methyl trough. Over 95% of the halothane molecules are located below the lipid carbonyl carbons, in agreement with photolabeling experiments. Halothane induces lateral expansion and a concomitant contraction in the bilayer thickness. A decrease in the acyl chain segment order parameters, S(CD), for the tail portion, and a slight increase for the upper portion compared to neat bilayers, are in agreement with several NMR studies on related systems. The decrease in S(CD) is attributed to a larger accessible volume per lipid in the tail region. Significant changes in the electric properties of the lipid bilayer result from the structural changes, which include a shift and broadening of the choline headgroup dipole (P-N) orientation distribution. Our findings reconcile apparent controversial conclusions from experiments on diverse lipid systems.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1998

Effects of anesthetics on the structure of a phospholipid bilayer: molecular dynamics investigation of halothane in the hydrated liquid crystal phase of dipalmitoylphosphatidylcholine.

We report the results of constant temperature and pressure molecular dynamics calculations carried out on the liquid crystal (Lalpha) phase of dipalmitoylphosphatidylcholine with a mole fraction of 6.5% halothane (2-3 MAC). The present results are compared with previous simulations for pure dipalmitoylphosphatidylcholine under the same conditions (Tu et al., 1995. Biophys. J. 69:2558-2562) and with various experimental data. We have found subtle structural changes in the lipid bilayer in the presence of the anesthetic compared with the pure lipid bilayer: a small lateral expansion is accompanied by a modest contraction in the bilayer thickness. However, the overall increase in the system volume is found to be comparable to the molecular volume of the added anesthetic molecules. No significant change in the hydrocarbon chain conformations is apparent. The observed structural changes are in fair agreement with NMR data corresponding to low anesthetic concentrations. We have found that halothane exhibits no specific binding to the lipid headgroup or to the acyl chains. No evidence is obtained for preferential orientation of halothane molecules with respect to the lipid/water interface. The overall dynamics of the lipid-bound halothane molecules appears to be reminiscent of that of other small solutes (Bassolino-Klimas et al., 1995. J. Am. Chem. Soc. 117:4118-4129).

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1997

Voltage-clamp analysis of halothane effects on GABA(A fast) and GABA(A slow) inhibitory currents.

Voltage-clamped GABA(A fast) and GABA(A slow) inhibitory postsynaptic currents (IPSCs) were selectively elicited in hippocampal area CA1 pyramidal neurons. Clinically relevant concentrations of halothane (1.2 vol.%) prolonged both GABA(A fast) and GABA(A slow) IPSC decay times approximately 2.5 fold, while having little to no effect on current amplitudes or rise times. Current-voltage analysis revealed that IPSC reversal potentials (-70 to -75 mV) remained constant in the presence of halothane. Under control conditions, GABA(A slow) IPSC decay times increased linearly with membrane depolarization, and this IPSC decay time voltage dependence was not significantly altered by halothane. These results confirm the existence of separable GABA(A fast) and GABA(A slow) IPSCs in hippocampus, and further elucidate the effects of halothane on these currents.

Anesthetics, General↗
PubMed1998

Halothane depresses action potential conduction in hippocampal axons.

General anesthetics are thought to depress the central nervous system (CNS) by acting at synapses; however, only a few studies have compared effects on axonal conduction with effects on synaptic responses using mammalian CNS preparations. The present study used glutamate receptor antagonists (CNQX/APV) or low calcium to block synaptic transmission, allowing Schaffer-collateral axon fiber volleys to be recorded from rat hippocampal brain slices. Since fiber volleys are compound action potentials, they provide a measure of axonal conduction in Schaffer-collateral fibers. Clinical concentrations of the inhalational anesthetic, halothane (1 rat MAC, 1.2 vol.%), produced an 18 +/- 2.3% depression of fiber volley amplitudes (mean +/- S.D.; p < 0.001 ANOVA, n = 10). Depression of action potential conduction accounted for approximately 30% of the overall depression of synaptic transmission produced by halothane at this concentration. Halothane-induced fiber volley depression occurred with little change in conduction velocity, similar to the effect seen with decreased stimulus intensity, but significantly different from the decreased velocity produced by tetrodotoxin (100 nM, p < 0.005). The results indicate that halothane can depress axonal conduction at clinically relevant concentrations and that this depression could contribute to the CNS depression that is associated with anesthesia.

Action Potentials↗
PubMed2000

Molecular dynamics simulation of four-alpha-helix bundles that bind the anesthetic halothane.

The mutation of a single leucine residue (L38) to methionine (M) is known experimentally to significantly increase the affinity of the synthetic four-alpha-helix bundle (Aalpha(2))(2) for the anesthetic halothane. We present a molecular dynamics study of the mutant (Aalpha(2)-L38M)(2) peptide, which consists of a dimer of 62-residue U-shaped di-alpha-helical monomers assembled in an anti topology. A comparison between the simulation results and those obtained for the native (Aalpha(2))(2) peptide indicates that the overall secondary structure of the bundle is not affected by the mutation, but that the side chains within the monomers are better packed in the mutant structure. Unlike the native peptide, binding of a single halothane molecule to the hydrophobic core of (Aalpha(2)-L38M)(2) deforms the helical nature of one monomer in a region close to the mutation site. Increased exposure of the cysteine side chain to the hydrophobic core in the mutant structure leads to the enhancement of the attractive interaction between halothane and this specific residue. Since the mutated residues are located outside the hydrophobic core the observed increased affinity for halothane appears to be an indirect effect of the mutation.

Amino Acid Sequence↗
PubMed1994

Effects of volatile anesthetics, enflurane, isoflurane, and halothane on ventricular delayed activation in a canine myocardial infarction model.

The authors examined the effects of volatile anesthetics (enflurane, isoflurane, and halothane) on ventricular activation in a canine myocardial infarction model. Enflurane at 1 minimum aveolar concentration further delayed or blocked delayed activation in the infarcted zones with only slight effects on activation of the normal zones. Halothane showed similar and comparable effects on ventricular activation to those of enflurane. Although isoflurane also showed similar effects, they were of a lesser extent. Enflurane and halothane, but not isoflurane, inhibited ventricular stimulation-induced arrhythmias. Thus, enflurane and halothane produced marked depression of delayed activation in myocardial infarction, which may affect, that is, inhibit or provoke, ventricular arrhythmias in myocardial infarction.

Animals↗
PubMedDate not supplied

Cardiopulmonary effects of sevoflurane in cats: comparison with isoflurane, halothane, and enflurane.

The cardiopulmonary effects of sevoflurane (mean, 2.6, 3.8-3.9 and 5.2 per cent) were compared with those of halothane (1.2, 1.8 and 2.4 per cent), enflurane (2.4, 3.6 and 4.8 per cent) and isoflurane (1.6, 2.4 and 3.2-3.3 per cent) at end-tidal concentrations equivalent to 1, 1.5 and 2 minimal alveolar concentrations (MACs) during spontaneous or controlled ventilation (SV or CV) in 57 cats. Cats were assigned to four groups of nine animals each in SV trial and four groups of five or six animals each in CV trial. During SV, respiration rate was decreased by sevoflurane and isoflurane at 2 MAC and by enflurane at each MAC multiple when compared with control values, whereas halothane increased respiration rate at 2 MAC. The degree of hypercapnia and acidosis induced by sevoflurane was not different from that induced by isoflurane and was less than that induced by halothane at 1 to 1.5 MAC or enflurane at 2 MAC. During SV and CV, four anaesthetics decreased heart rate at 2 MAC when compared with control values, but there was no significant difference between anaesthetics. Sevoflurane, like halothane and isoflurane, induced hypotension at 2 MAC when compared with 1 MAC.

Anesthetics, Inhalation↗
PubMedDate not supplied

Changes in plasma cortisol concentrations in bitches in response to different combinations of halothane and butorphanol, with or without ovariohysterectomy.

Changes in plasma cortisol concentrations were assessed in bitches in response to nine treatments: control, anaesthesia, analgesia, analgesia followed by anaesthesia, anaesthesia followed by analgesia at intubation, anaesthesia followed by analgesia at extubation, anaesthesia plus surgery, analgesia followed by anaesthesia plus surgery, and anaesthesia plus surgery followed by analgesia. The anaesthetic was halothane, the analgesic was butorphanol (0.4 mg kg(-1)) and the surgery was ovariohysterectomy. Blood samples, for plasma cortisol assays, were taken regularly from before treatment for five hours and then again after 24 hours. A small transient rise in plasma cortisol concentration in the control group was attributed to mild distress associated with novel experiences. A more pronounced and protracted rise in cortisol concentration in the analgesia group was ascribed to a dysphoric state of bitches under the influence of the agonist-antagonist butorphanol. Halothane anaesthesia alone resulted in no change in plasma cortisol concentration. When butorphanol was given after anaesthesia was induced or while the animal was still under the influence of anaesthesia (immediately after tracheal extubation), there was no immediate rise in plasma cortisol concentration and low concentrations were maintained for up to 60 minutes after halothane withdrawal. A marked rise in plasma cortisol concentration, which was sustained above pretreatment values for at least five hours, occurred in all surgery groups. Giving intravenous butorphanol 30 minutes prior to surgery had no effect on the surgically-induced rise in plasma cortisol concentration and no effect on the postsurgical plasma cortisol concentration. In contrast, butorphanol given at extubation did reduce plasma cortisol concentrations during the postsurgical period. These observations did not support the hypothesis that preoperative use of butorphanol would reduce the cortisol response after surgery under halothane anaesthesia.

Analgesia↗