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PubMed1995

Sevoflurane versus halothane for general anesthesia in pediatric patients: a comparative study of vital signs, induction, and emergence.

STUDY OBJECTIVE: To compare vital signs and the speed of induction and emergence with sevoflurane versus halothane in pediatric patients. DESIGN: Prospective, randomized, open study. SETTING: Thomas Jefferson University Hospital. PATIENTS: 40 unpremedicated ASA Physical Status I and II children age 9 months to 16 years undergoing elective inpatient otorhinolaryngologic or orthopedic surgery. INTERVENTIONS: Standardized induction of anesthesia with sevoflurane (start: 1%, maximum: 7%) or halothane (start: 0.5%, maximum: 5%) in nitrous oxide/oxygen (N2O/O2). Intubation following vecuronium and 4 minutes of controlled ventilation with 2 minimum alveolar concentration (MAC) drug in O2; 1.5 MAC drug in N2O/O2 delivered for 20 minutes; then 0.75 MAC until the end of surgery. Fentanyl 1 mcg/kg was administered 15 minutes before the anticipated end of surgery, at which time anesthetics were stopped and mechanical ventilation continued until eye opening (emergence). MEASUREMENTS AND MAIN RESULTS: Blood pressure, heart rate (HR), oxygen saturation, end-tidal gas concentrations, and temperature were recorded. Induction and emergence times were measured to the nearest second. Induction (loss of eyelash reflex) was faster with sevoflurane (97 +/- 31 sec) than halothane (120 +/- 36 sec; p < 0.05), despite a lower inspired sevoflurane MAC. Emergence was faster with sevoflurane (9.9 +/- 2.9 min vs. 12.5 +/- 4.7 min; p < 0.05), despite a higher MAC multiple of end-tidal sevoflurane concentration at the end of surgery. Following intubation, HR (compared with the preinduction value in the operating room) was significantly higher in the halothane group (136.8% +/- 16.3% vs. 115.0% +/- 25.6%), as was mean arterial pressure (113.2% +/- 25.5% vs. 87.8% +/- 22.6%). This finding corresponded with a higher MAC multiple of end-tidal concentration in the sevoflurane group than in the halothane group. CONCLUSIONS: Induction of and emergence from anesthesia was faster with sevoflurane than halothane. Airway complications were low in both groups. Vital signs were more stable with sevoflurane during induction through intubation, and were comparable during maintenance. Sevoflurane is an excellent drug for inhalational induction in pediatric patients.

Adolescent↗
PubMed2004

Inhibitory effects of halothane on the thermogenic pathway in brown adipocytes: localization to adenylyl cyclase and mitochondrial fatty acid oxidation.

Volatile anesthetics such as halothane efficiently inhibit nonshivering thermogenesis as well as the cellular manifestation of that phenomenon: norepinephrine-induced respiration in brown adipocytes. To identify the molecular site(s) of action of such anesthetics, we have examined the effect of halothane on the sequential intracellular steps from the interaction of norepinephrine with isolated brown adipocytes to the stimulation of mitochondrial respiration (=thermogenesis). We did not identify an inhibition at the level of the adrenergic receptors, but a first site of inhibition was identified as the generation of cAMP by adenylyl cyclase; this led to inhibition of norepinephrine-induced expression of the uncoupling protein-1 (UCP1) gene and reduced norepinephrine-induced lipolysis as secondary effects. Although an inhibition of lipolysis in itself would inhibit thermogenesis, circumvention of this inhibition revealed that a second, postlipolytic, site of inhibition existed: halothane also inhibited the stimulatory effect of exogenous fatty acids on cellular respiration. This inhibition was independent of the presence of UCP1 in the mitochondria of the cells and was thus not directly on the thermogenic uncoupling mechanism. Since not only fatty acid oxidation but also pyruvate oxidation were inhibited by halothane in isolated mitochondria, whereas glycerol-3-phosphate oxidation was not, the second site of action of halothane, evident when cyclase/lipolytic inhibition was circumvented, was located to the respiratory chain, complex I. The results thus explain the inhibition of nonshivering thermogenesis by identifying two sites of action of halothane in brown adipocytes. In addition, the results may open for new formulations of the molecular background to anesthesia.

Adenylyl Cyclases↗
PubMed2004

Blood flow-dependent changes in intrarenal nitric oxide levels during anesthesia with halothane or sevoflurane.

We previously demonstrated that intrarenal nitric oxide (NO) levels and renal blood flow are reduced during halothane anesthesia. Studies were performed to determine if volatile anesthetics-induced reductions in renal NO levels are associated with blood flow changes. Halothane and sevoflurane at 0.8 and 2.4 Mac were administered by inhalation to dogs, and cGMP and NOx concentrations in the renal interstitial fluid were measured by a microdialysis method. Neither halothane nor sevoflurane at 0.8 Mac altered renal blood flow and renal interstitial cyclic guanosine monophosphate (cGMP) and NOx levels, but both anesthetics significantly decreased these values at 2.4 Mac. Using an adjustable aortic clamp, renal perfusion pressure was reduced in 2 steps without halothane and sevoflurane anesthesia. Renal blood flow as well as cGMP and NOx concentrations in the renal interstitial fluid were unchanged within the autoregulatory range, but significantly decreased below the autoregulatory range. Changes in cGMP and NOx concentrations in the renal interstitial fluid were highly correlated with renal blood flow changes during halothane or sevoflurane anesthesia, and during stepwise reductions in renal perfusion pressure. The results suggested that halothane- and sevoflurane-induced decreases in intrarenal NO levels result from reductions in blood flow.

Anesthetics, Inhalation↗
PubMed2005

Effects of inhalation anesthetics halothane, sevoflurane, and isoflurane on human cell lines.

Cytotoxic and antiproliferative effects of halothane, isoflurane, and sevoflurane in anesthetic doses on human colon carcinoma (Caco-2), larynx carcinoma (HEp-2), pancreatic carcinoma cells (MIA PaCa-2), poorly differentiated cells from lymph node metastasis of colon carcinoma (SW-620), and normal fibroblasts were investigated. Cells were exposed to anesthetic gas mixture consisting of O(2): N2O (35:60 vol.%), halothane (1.5 vol.%) or isoflurane (2.0 vol.%) or sevoflurane (3.0 vol.%), and CO(2) (5 vol.%), for 2, 4, and 6 h. Cytotoxicity of anesthetics was analyzed by validated tetrazolium dye assay MTT test. All anesthetics expressed cytotoxic effects on treated tumor cells in time and cell line dependent manner. Growth suppression in cells exposed to halothane was enhanced in HEp-2 (to 67.7%), Caco-2 (to 76.3%), and SW620 cells (to 80.9%), and was minimal in normal fibroblasts (to 89.4%). Antiproliferative activity of halothane was measured via radioactive precursors incorporation assay. In Caco-2 cells treated by halothane, decrease in DNA synthesis (52.4%, p=0.001), RNA synthesis (39.2%, p<0.001), and protein synthesis (19.2%, p=0.004) was observed. In HEp-2 cells, DNA and RNA syntheses were decreased to 72.5% and 79.9%, whereas protein synthesis was 14.0% of control (p<0.001). In SW620 cells, protein synthesis after 4 h was 24.4% (p=0.007). A DNA fragmentation was observed in Caco-2 and MIA PaCa-2 cells. Exposition of phosphatidylserine on outer lipid bilayer plasma membrane of tumor cell treated by halothane proved apoptosis as mode of cell death.

Anesthetics, Inhalation↗
PubMed2005

Confounding effects of anesthesia on functional activation in rodent brain: a study of halothane and alpha-chloralose anesthesia.

Functional magnetic resonance imaging (fMRI) in animal models provides a platform for more extensive investigation of drug effects and underlying physiological mechanisms than is possible in humans. However, it is usually necessary for the animal to be anesthetized. In this study, we have used a rat model of direct cortical stimulation to investigate the effects of anesthesia in rodent fMRI. Specifically, we have sought to answer two questions (i) what is the relationship between baseline neuronal activity and the BOLD response to stimulation under halothane anesthesia? And (ii) how does the BOLD response change after transferring from halothane to the commonly used anesthetic alpha-chloralose? In the first set of experiments, we found no significant differences in the amplitude of the BOLD response at the different halothane doses studied, despite electroencephalography (EEG) recordings indicating a dose-dependent reduction in baseline neuronal activity with increasing halothane levels. In the second set of experiments, a reduction in the spatial extent of the BOLD response was apparent immediately after transfer from halothane to alpha-chloralose anesthesia, although no change in the peak signal change was evident. However, several hours after transfer to alpha-chloralose, a significant increase in both the spatial extent and peak height of the BOLD response was observed, as well as an increased sensitivity to secondary cortical and subcortical activation. These findings suggest that, although alpha-chloralose anesthesia is associated with a greater BOLD response for a fixed stimulus relative to halothane, there is substantial variation in the extent and magnitude of the response over time that could introduce considerable variability in studies using this anesthetic.

Anesthesia, General↗
PubMed1999

Drastic increase in nitric oxide content in rat brain under halothane anesthesia revealed by EPR method.

A drastic increase in nitric oxide (NO) content was revealed by the EPR method in rat brain cortex and cerebellum under halothane anesthesia. The NO scavenger diethyldithiocarbamate sodium salt (DETC) and ferrous citrate were injected into adult rats 30-60 min before anesthesia. Rats were anesthetized by inhalation of a halothane-oxygen mixture (1%, 1.5%, 2%, or 4%). After different times of anesthesia, rats were decapitated, and brain cortex and cerebellum were dissected, frozen in liquid nitrogen, and subjected to EPR spectroscopy. The concentration of NO was determined from the NO-Fe-DETC radical spectrum. In control animals, NO content in the cerebellum was only 68% of that in the cortex. We observed a time-dependent increase in NO content in the cortex and cerebellum of rats anesthetized with 1.5% halothane. In brain cortex, the NO level increased to six times that of waking animals after 30 min and remained at this level up to 60 min of anesthesia. In cerebellum the changes were less drastic, the NO level showing only a 2-fold increase. The same effect was produced by 1% and 2% halothane. Ketamine, chloral hydrate, and pentobarbital were used as reference drugs. None of these anesthetics produced effects similar to those of halothane. In ketamine-anesthetized rat brain, the NO content slightly decreased. Pentobarbital and chloral hydrate produced an insignificant increase in NO. Data are discussed in the context of possible interference of halothane in the regulation of nitric oxide synthase activity.

Adjuvants, Anesthesia↗
PubMed2000

Prevention of halothane-induced hepatotoxicity by hemin pretreatment: protective role of heme oxygenase-1 induction.

Reductive metabolism of halothane in phenobarbital-pretreated rats is known to increase free radical formation that results in hepatotoxicity. It also is associated with a marked induction of microsomal heme oxygenase-1 (HO-1), suggesting that there is an alteration in heme metabolism. In this study, we examined heme metabolism in rats pretreated with phenobarbital, followed by exposure to halothane-hypoxia. In this model, there was a significant decrease in microsomal cytochrome P450 content in the liver, followed by a rapid increase in free heme concentration and a decrease in the level of mRNA for the nonspecific delta-aminolevulinate synthase. A transient but dramatic induction of HO-1 mRNA and a prolonged induction of heat shock protein 70 mRNA also occurred. The HO-1 protein was detected principally in the hepatocytes around the central vein. Serum alanine transaminase (ALT) activity, an indicator of hepatic dysfunction, increased continuously throughout the experiment. Hemin pretreatment induced hepatic HO-1 with abrogation of the halothane-induced hepatotoxicity in this model, as judged by ALT activity and normal histology. Our findings in this study thus indicate that halothane-induced hepatotoxicity is due not only to its reductive metabolite formation, but also to an increase in hepatic free heme concentration, which is a potent prooxidant; HO-1 induction is an important protective response against such changes. This is also the first study to demonstrate that hemin pretreatment, which induces HO-1 prior to exposure to halothane, effectively prevents halothane-induced hepatotoxicity.

5-Aminolevulinate Synthetase↗
PubMed1998

Differential halothane binding and effects on serum albumin and myoglobin.

To understand further the weak molecular interactions between inhaled anesthetics and proteins, we studied the character and dynamic consequences of halothane binding to bovine serum albumin (BSA) and myoglobin using photoaffinity labeling and hydrogen-tritium exchange (HX). We find that halothane binds saturably and with submillimolar affinity to BSA, but either nonspecifically or with considerably lower affinity to myoglobin. Titration of halothane binding with guanidine hydrochloride suggested more protection of binding sites from solvent in BSA as compared with myoglobin. Protection factors for slowly exchanging albumin hydrogens are increased in a concentration-dependent manner by up to 27-fold with 10 mM halothane, whereas more rapidly exchanging groups of albumin hydrogens have either unaltered or decreased protection factors. Protection factors for slowly exchanging hydrogens in myoglobin are decreased by halothane, suggesting destabilization through binding to an intermediate or completely unfolded conformer. These results demonstrate the conformation dependence of halothane binding and clear dynamic consequences that correlate with the character of binding in these model proteins. Preferential binding and stabilization of different conformational states may underlie anesthetic-induced protein dysfunction, as well as provide an explanation for heterogeneity of action.

Affinity Labels↗
PubMed2001

Halothane-induced intracellular calcium release in cholinergic cells.

Low concentrations of halothane and isoflurane can release acetylcholine in an extracellular Ca(2+)-independent manner. In the present study, a cholinergic cell line (SN56) was used to examine whether release of calcium from intracellular stores occurs in the presence of halothane. Changes in intracellular calcium concentration ([Ca(2+)](i)) were measured using fluo-3, a fluorescent calcium-sensitive dye and laser scanning confocal microscopy. Halothane, at sub-anesthetic concentrations (14, 28, 40 and 56 microM), increased [Ca(2+)](i) in SN56 cells. This effect remained even when the cells were perfused with medium lacking extracellular calcium, suggesting the involvement of intracellular Ca(2+) sources. SN56 cells responded to ryanodine by increasing [Ca(2+)](i) and this effect was blocked by dantrolene, an inhibitor of Ca(2+)-release from ryanodine-sensitive stores. The effect of halothane was attenuated after the increase in [Ca(2+)](i) induced by ryanodine and it was suppressed by dantrolene, suggesting the participation of ryanodine-sensitive stores. Using cyclopiazonic acid, a Ca(2+)-ATPase inhibitor, we investigated whether the depletion of intracellular Ca(2+) stores interfered with the effect of halothane. Cyclopiazonic acid significantly decreased the increase in [Ca(2+)](i) induced by the volatile anesthetic. It is suggested that sub-anesthetic concentrations of halothane may increase [Ca(2+)](i) by releasing Ca(2+) from intracellular stores in cholinergic cells.

Acetylcholine↗
PubMed1997

Dexmedetomidine and halothane produce similar alterations in electroencephalographic and electromyographic activity in cats.

Dexmedetomidine, an alpha2-adrenergic agonist, produces sedation and reduces volatile anesthetic requirements. This investigation compared the actions of dexmedetomidine and halothane on the processed EEG and on the electromyogram (EMG) which has not been previously described. Chronically instrumented cats were prepared with arterial and venous cannulae, quadriceps EMG electrodes and EEG electrodes in the lateral geniculate nucleus and over the frontal and occipital cortices. Hemodynamics, EEG and EMG were recorded in the conscious state and after randomly administered halothane or intravenous dexmedetomidine (on separate days). Blink and tail-clamp responses also assessed level of consciousness. Halothane resulted in unconsciousness and a lack of response to tail clamping, while dexmedetomidine produced profound sedation, with preservation of tail-clamp responses. Both agents similarly decreased (P < 0.05) the median power frequency from 9.5 +/- 0.9 to 5.7 +/- 0.4 Hz (2% halothane) and from 9.6 +/- 0.7 to 5.9 +/- 0.8 Hz (20 microg/kg dexmedetomidine), and 95% power frequency from 23.0 +/- 0.2 to 18.2 +/- 0.6 Hz (2% halothane) and from 23.0 +/- 0.2 to 19.1 +/- 0.8 Hz (20 microg/kg dexmedetomidine). Both agents increased the total spectral power and delta band power of the EEG and reduced integrated EMG activity. Halothane and dexmedetomidine produced differing effects on level of consciousness as assessed by response to tail clamping. The results suggest that conventional processing of EEG and EMG parameters are inadequate to assess anesthetic depth in the presence of alpha2-adrenergic agonists.

Adrenergic alpha-Agonists↗
PubMed1998

Interindividual variability in P450-dependent generation of neoantigens in halothane hepatitis.

Halothane hepatitis occurs because susceptible patients mount immune responses to trifluoroacetylated protein antigens, formed following cytochrome P450-mediated bioactivation of halothane to trifluoroacetyl chloride. In the present study, an in vitro approach has been used to investigate the cytochrome P450 isozyme(s) which catalyze neoantigen formation and to explore the protective role of non-protein thiols (cysteine and reduced glutathione). Significant levels of trifluoroacetyl protein antigens were generated when human liver microsomes, and also microsomes from livers of rats pre-treated with isoniazid, phenobarbital or beta-naphtoflavone, were incubated with halothane plus a nicotinamide adenine dinucleotidephosphate (NADPH) generating system. Immunoblotting studies revealed that the major trifluoroacetyl antigens expressed in vitro exhibited molecular masses of 50-55 kDa and included 60 and 80 kDa neoantigens recognized by antibodies from patients with halothane hepatitis. Much lower concentrations of halothane were required to produce maximal antigen generation in isoniazid-induced rat microsomes, as compared with phenobarbital or isosafrole-induced microsomes (0.5 vs 12.5 microl/ml). In isoniazid-induced microsomes, antigen generation was inhibited > 90% by the nucleophiles cysteine and glutathione and by the CYP2E1-selective inhibitors diallylsulfide and p-nitrophenol, but was unaffected by inhibitors of other P450 isozymes (furafylline, sulfaphenazole or triacetyloleandomycin). Neoantigen formation in six human liver microsomal preparations was inhibited in the presence of diallylsulfide, but not by furafylline, sulfaphenazole or triacetyloleandomycin, and exhibited marked variability which correlated with CYP2E1 levels. These results suggest that the balance between metabolic bioactivation by CYP2E1 and detoxication of reactive metabolites by cellular nucleophiles could be an important metabolic risk factor in halothane hepatitis.

Animals↗
PubMed2002

Halothane attenuates the cerebroprotective action of several Na+ and Ca2+ channel blockers via reversal of their ion channel blockade.

We have previously shown the involvement of Na(+) channel as well as N-type and P/Q-type Ca(2+) channels in the oxygen and glucose deprivation-induced injury in rat cerebrocortical slices. In the present study, we investigated the influence of halothane on the cerebroprotective effects of a variety of Na(+) and Ca(2+) channel blockers in rat cerebrocortical slices. The hypoxic injury was attenuated by Na(+) channel blockers including tetrodotoxin, lidocaine and dibucaine, and Ca(2+) channel blockers, such as verapamil, omega-agatoxin IVA and omega-conotoxin GVIA. Halothane abolished the protective effects of lidocaine, dibucaine and verapamil, all of which block the respective cation channels in a voltage-dependent manner, without affecting the actions of tetrodotoxin, omega-agatoxin IVA and omega-conotoxin GVIA, which reveal voltage-independent blockade. On the other hand, the nitric oxide synthesis estimated from the extracellular cyclic GMP formation was elevated during exposure to hypoxia. All channel blockers tested here attenuated hypoxia-evoked nitric oxide synthesis. Halothane blocked almost completely these actions of lidocaine and verapamil. Moreover, the Na(+) and Ca(2+) channel blockade by these compounds, as determined by veratridine- and KCl-stimulated nitric oxide synthesis, respectively, was also reversed by halothane. These findings suggest that an anesthetic agent halothane reversed the Na(+) and Ca(2+) channel blockade of several voltage-dependent ion channel blockers, leading to the attenuation of their cerebroprotective actions. Therefore, the influence of halothane anesthesia should be taken into consideration for the evaluation of neuroprotective action of Na(+) and Ca(2+) channel blockers.

Animals↗
PubMed1996

Halothane counteracts acetylcholine-induced increase in Ca2+ sensitivity of the contractile apparatus in airway smooth muscle.

The direct relaxing effect of halothane on airway smooth muscle has been reported to involve the reduction of the cytosolic Ca2+ concentration ([Ca2+]i) and the [Ca2+]i-independent inhibitory mechanism. To clarify the extent of the contribution of these mechanisms, the effect of halothane on the [Ca2+]i-tension relationship in porcine tracheal smooth muscle strips was evaluated, using fura-2 fluorometry. The control [Ca2+]i-tension relationship was constructed from data of [Ca2+]i and tension during the contractions induced by the stepwise increment of extracellular Ca2+ concentrations under high K+ depolarization. In the presence of acetylcholine (1 microM), the [Ca2+]i-tension relationship shifted upward, which indicated the acetylcholine-induced increase in the Ca2+ sensitivity of the contractile apparatus. Halothane (0.034 mM), in the absence of acetylcholine, did not alter the increases in either [Ca2+]i or tension, hence no change in the [Ca2+]i-tension relationship. However, in the presence of acetylcholine, halothane did attenuate the acetylcholine-induced upward shift of the [Ca2+]i-tension relationship. Halothane proved to have a potent attenuating effect on the acetylcholine-induced increase in Ca2+ sensitivity of the contractile apparatus with little influence on [Ca2+]i. This desensitization of the contractile apparatus to [Ca2+]i may play a major role in the direct airway relaxing effect of halothane.

Acetylcholine↗
PubMed1997

Heterogeneous halothane binding in the SR Ca2+-ATPase.

The activity of various Ca2+-ATPases is affected by volatile anesthetics, such as halothane, commonly used in clinical practice. The effect on the enzyme in skeletal muscle sarcoplasmic reticulum (SR) is biphasic, including stimulation at clinical anesthetic concentrations and subsequent inhibition at higher concentrations. We have previously proposed that the action of a volatile anesthetic on Ca2+-ATPases results from its binding in the interior of the enzyme molecule [Lopez, M.M. and Kosk-Kosicka, D. (1995) J. Biol. Chem. 270, 28239-28245]. Presently, we investigated whether the anesthetic interacts directly with the skeletal muscle SR Ca2+-ATPase (SERCA1) as evidenced by binding. Photoaffinity labeling with [14C]halothane demonstrated that the anesthetic binds saturably to SR membranes, and that approximately 80% of the binding is specific, with a KI of 0.6 mM. The KI value agrees well with the concentration at which halothane half-maximally activates SERCA1. SDS gel electrophoresis of labeled membranes indicates that 38-56% of [14C]halothane incorporates into SERCA1, and 38-53% in lipids. Distribution of label among the three fragments produced by controlled tryptic digestion of SERCA1 suggests heterogeneous halothane binding presumably in discrete sites in the enzyme. The results provide the first direct evidence that halothane binds to SERCA1. Potentially this binding could be related to anesthetic effect on enzyme's function.

Binding Sites↗
PubMedDate not supplied

Inhalatory anesthetic (halothane) associated changes in the immune response in mice.

The extent of surgery, the patient's age, health status and other factors may contribute to alteration of the immune system during anesthesia and surgery. In addition, inhalatory anesthetics may cause acute and chronic toxicity because of the production of intermediate and end metabolic compounds. The present work was undertaken to evaluate, both in vivo and in vitro, if repeated doses of halothane were able to affect the immune response in a murine model developed at our laboratory. Weekly doses of halothane were administered to mice subjected to no surgery and three days after the last anesthetic-exposure, several immunologic parameters were assessed. Results on the in vivo response to sheep red blood cells showed that halothane treatment increased the amount of specific antibody secreting B-cells, without affecting the delayed type hypersensitivity reaction to the same antigen. In vitro studies on spleen cell composition showed that halothane re-exposure diminished the number of CD4+, CD8+ and B-cells. Such changes were not translated into alterations on the mitogen-driven lymphoproliferation, as well as macrophage phagocytic and lytic functions. Our results indicate that halothane re-exposure is able to modulate the immune response affecting both the number of antibody secreting cells involved in a specific in vivo response, and the splenic lymphoid cell composition. Since such halothane-induced immune alterations might bias the results of a wide range of physiological research, even those involving other systems, a careful selection of the anesthetic agent and methods by which the compound is administered is advisable.

Anesthetics, Inhalation↗
PubMed1993

[Effects of isoflurane and halothane on motor evoked potentials in the rabbit].

The effects of isoflurane or halothane on motor evoked potentials (MEPs) were assessed and compared in the rabbit, in order to contribute to devise a rigorous human anaesthetic protocol to be used for monitoring of MEPs in corrective spinal surgery. Ten black adult New Zealand rabbits were anaesthetised twice at a month interval, once with isoflurane and once with halothane. Once a control cortical stimulation had been carried out after the animal had breathed pure oxygen for three minutes, the following concentrations of anaesthetic agent were given for 3 min each: respectively 0.3 vol %, 0.5 vol % and 1 vol % of isoflurane, and 0.5 vol % and 1 vol % of halothane. Cortical stimulation was carried out every minute. The signs of anaesthesia (diameter decrease of the pupil, eye covered by the nictating membrane), muscle relaxation (ears drop) and breathing rate were recorded. MEPs were recorded 1, 2, 3 and 5 minutes after the end of anaesthesia. Isoflurane had a stronger effect on MEPs than halothane. The effect was more pronounced on amplitude than on latency. MEPs remained present whatever the concentration of halothane. In 70% of cases, MEPs, discontinued with isoflurane, more rapidly, more deeply, and for a longer time. Mean latency was more constantly increased in the isoflurane than in the halothane group. The effect of volatile halogenated anaesthetics on mean latency of MEPs seemed to be more delayed than that on amplitude. One should also take into account an individual sensitivity, it is concluded that the interpretation of MEPs during anaesthesia with volatile halogenated agents should be carried out with caution.

Anesthesia, Inhalation↗
PubMed2000

Pharmacodynamics and intubating conditions of cisatracurium in children during halothane and opioid anesthesia.

STUDY OBJECTIVES: To determine the pharmacodynamics and intubating conditions of cisatracurium 0.2 mg/kg in children aged 2 to 12 years. DESIGN: Open-label, randomized study. SETTING: Operating room of a university-affiliated hospital. PATIENTS: 42 ASA physical status I and II patients, 24 to 155 months of age. INTERVENTIONS: Patients were assigned to one of two groups: halothane anesthesia (G1) and opioid anesthesia (G2). Subsequently, each group was divided into two age subgroups: 24-59 months and 60-155 months. All patients were premedicated with midazolam intranasal 0.1 to 0.2 mg/kg. In G1, anesthesia was induced with halothane up to 3% and N(2)O/O(2) (60-70/30-40%). Halothane was reduced to </=2%, 2 minutes before cisatracurium was administered. In G2, anesthesia was induced with fentanyl 2 mcg/kg and thiopental 5 mg/kg. Anesthesia was maintained with halothane 0.8-1.5% in N(2)O/O(2) in G1, and it was maintained with fentanyl, thiopental, and N(2)O/O(2) in G2. Electromyography (EMG) assessed the neuromuscular function of the adductor pollicis every 10 seconds with single-twitch supramaximal stimulus at induction and train-of-four at recovery. After obtaining EMG baseline, cisatracurium was administered. Onset time, time to 90% block, percentage of maximal block, clinical duration, and intubating conditions were recorded. For statistical analysis, Chi-square test, analysis of variance, and Tukey's test were used, with p-value less than 0.05. MEASUREMENTS AND MAIN RESULTS: Only first twitch (T(1)) recovery to 25% was significantly longer in patients aged 24 to 59 months who received halothane-based anesthesia, compared with those who received opioid-based anesthesia (p < 0.05). Onset time, maximum block, and intubating conditions did not differ between groups (p > 0.05). CONCLUSIONS: Cisatracurium 0.2 mg/kg offered acceptable intubating conditions at 90 seconds in 98% of pediatric patients, regardless of the anesthesia-based technique. Longer clinical duration in the halothane group in younger children may be due to age-related potentiation or to the small number of patients enrolled in the younger subgroup.

Anesthesia↗
PubMed1997

Pulmonary microvascular injury following general anaesthesia with volatile anaesthetics--halothane and isoflurane: a comparative clinical and experimental study.

Pulmonary microvascular injury has become a recently studied phenomenon that may be responsible for most of the complications associated with the lungs. Thirty patients undergoing partial hemilaminectomy or discectomy due to hernia of nucleus pulposus underwent Tc-99m HMPAO lung clearance as well as Tc-99m pertechnetate lung scintigraphy pre-operatively, and following general anaesthesia with halothane and isoflurane (third, fourth and tenth post-operative days). The results were compared with conventional techniques and haemodynamic parameters during the peri-operative period. In order to demonstrate acute phase changes under general anaesthesia and to perform pathological examinations, 21 New Zealand rabbits underwent radionuclide studies with Tc-99m HMPAO or Tc-99m pertechnetate. Lung biopsies were also performed. Despite no significant differences in any of the conventional diagnostic techniques, Tc-99m pertechnetate lung scintigraphy was performed for both the halothane and isoflurane groups, and Tc-99m HMPAO lung clearance was performed for the isoflurane group pre- or post-operatively. Tc-99m HMPAO lung clearance was impaired significantly in the halothane group on the third post-operative day (half time: 6.4 +/- 1.6 pre-operative and 13.76 +/- 3.3 s, P < 0.001) decreasing to pre-operative levels on the tenth post-operative day. Acute phase exposure to halothane was characterized with extremely abnormal Tc-99m HMPAO lung clearance in rabbits with respect to isoflurane, diminishing to control levels on the third day (half time: 8.7 +/- 86 control and 28.65 +/- 4.6, P < 0.001). Pathological examinations also demonstrated endothelial damage on acute exposure in the halothane group. General anaesthesia with halothane may give rise to alveolar microvascular injury, which generally seems to be underdiagnosed and may lead to serious post-operative complications.

Adult↗