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PubMed1980

[The influence of adrenaline on the effects of halothane and enflurane on the myocardium. Papillary muscle of the cat (author's transl)].

In this paper the influence of epinephrine on the isolated papillary muscle has been investigated with respect to the myocardial effects of enflurane and halothane. The contractile properties have been described under isotonic conditions by the parameters "muscle length change", "velocity of shortening and under isometric conditions by the parameters "peak tension" and "maximum rate of tension development". The studies led to the following results: 1. Halothane and enflurane cause a dose-dependent decrease of the contractile properties of the cat papillary muscle. Averaged for all parameters the mycocardial depressant effect of halothane is 2.6 times higher than that of enflurane, referring to equal concentrations. 2. Epinephrine has a positive inotropic effect which is most pronounced under isotonic mode of contraction for "velocity of shortening" and during isometric conditions for "maximum rate of tension development". 3. The positive inotropic effect of epinephrine is partially neutralized by halothane and enflurane. There is, however, evidence that the relative decrease of contractility due to halothane and enflurane is diminished by epinephrine. This finding shows that the myocardial effects of inhalation anaesthetics are overestimated in in-vitro-experiments (because of the lack of exogenous epinephrine) in contrast to experiments with intact animals. As this finding is referring to both halothane and enflurane, there is no specific difference to be found concerning the myocardial effects in comparative studies, including both in-vitro and in-vivo conditions.

Animals↗
PubMed1993

Selective inhibition of pressor and haemodynamic effects of NG-nitro-L-arginine by halothane.

We investigated the characteristics of inhibition by halothane of the pressor responses to NG-substituted L-arginine derivatives, nitric oxide (NO) synthase inhibitors. Intravenous (i.v.) bolus injections of NG-nitro-L-arginine (L-NNA, 1-32 mg/kg), NG-nitro-L-arginine methyl ester (L-NAME, 0.4-12.8 mg/kg), norepinephrine (NE, 0.25-8 micrograms/kg) and angiotensin II (AII, 0.02-0.64 micrograms/kg) each caused dose-dependent pressor responses in conscious rats. Halothane attenuated responses to the highest dose of NE and AII by approximately 18% but completely abolished responses to L-NNA and L-NAME. The haemodynamic effects of L-NNA were further examined by the microsphere technique in two groups of conscious rats and two groups of halothane-anaesthetized rats. An i.v. bolus injection of L-NNA (16 mg/kg) in conscious rats increased mean arterial pressure (MAP) and total peripheral resistance (TPR) and reduced heart rate (HR) and cardiac output (CO). These changes were associated with reduced conductance in all vascular beds, with the greatest reduction in the lungs and the least in the liver. In halothane-anaesthetized rats, L-NNA caused significant but markedly less change in MAP, HR, TPR, and CO as compared with those in conscious rats. The vasoconstrictor effects of L-NNA were attenuated by halothane in all beds except liver and spleen, with the greatest inhibition in heart. Our results suggest that NO plays a role in maintenance of peripheral vascular resistance and that halothane selectively and "noncompetitively" inhibits the vasoconstrictor effects of NO synthase inhibitors.

Amino Acid Oxidoreductases↗
PubMed1994

Time course of 72-kilodalton heat shock protein induction and appearance of trifluoroacetyl adducts in livers of halothane-exposed rats.

Previous studies have shown that exposure of phenobarbital-pretreated rats to halothane in 10% O2 causes centrilobular necrosis, induces expression of the 72-kDa heat shock protein (HSP72), and produces several trifluoroacetylated adducts. In the present study the time course of development of the centrilobular lesion, as measured by histochemistry, was compared with the time course of appearance of both trifluoroacetylated adducts and HSP72, as measured by Western blotting. One group of 20 rats was pretreated with phenobarbital for 5 days, whereas a second group of two rats was left as untreated controls. Ten phenobarbital-pretreated rats were exposed for 2 hr to 1% halothane in 10% O2 and 10 were exposed to 1% halothane in 20% O2. At either 2, 4, 6, or 24 hr after exposure, livers were excised and frozen without fixation. Thin sections stained with hematoxylin and eosin demonstrated that centrilobular lesions occurred at 6 hr and became extensive at 24 hr in rats pretreated with phenobarbital and exposed to 1% halothane in 10% O2. The time course of appearance of both trifluoroacetylated adducts and HSP72 was determined by Western blotting. Trifluoroacetylated adducts appeared in all rats exposed to halothane by 2 hr, lasted until 6 hr, and then diminished by 24 hr. In contrast, HSP72 was induced only in the rats pretreated with phenobarbital and exposed to 1% halothane in 10% O2. HSP72 appeared in both the nuclear and supernatant fractions at 6 hr after exposure and was intense 24 hr after exposure.

Animals↗
PubMed1994

[Hemodynamic effects of propafenone in dogs anesthesized with halothane or isoflurane].

OBJECTIVE: Several studies suggest that anaesthetic drugs influence the haemodynamic effects of the antiarrhythmic drugs. The aim of this study was to compare the haemodynamic effects of a standard dose of propafenone (1.5 mg/kg) on dogs anaesthetized with halothane or with isoflurane. DESIGN: Randomized laboratory animal study. MATERIAL AND METHODS: Six dogs were anaesthetized with 1% of halothane-Group I, and six dogs with an equianaesthetic dosage of isoflurane (1.5%)-Group II. Dogs breathed in spontaneous ventilation. Haemodynamic monitoring was performed with a femural arterial catheter and a flow-directed pulmonary artery catheter and cardiac output was measured by thermodilution. After a haemodynamic assessment considered as initial a bolus of 1.5 mg/kg of propafenone was given during a period of 30 seconds and similar assessments were made 5, 15, 30 and 60 minutes after. RESULTS: Before propafenone, heart rate was significantly higher in Group II-isoflurane (p < 0.05). After propafenone we found: In both Groups, a decrease in the cardiac output (p < 0.05) with the mean arterial pressure maintained; in Group I (halothane) a decrease in the stroke volume (p < 0.05) which was not found in Group II (p = ns); In Group II (isoflurane) a decrease in heart rate (p < 0.05) not found in Group I (p = ns). All the changes were higher at the 5th minute values. 30th minute and 60th minute values were not significantly different from initial values. CONCLUSION: In dogs anaesthetized with halothane 1.2 MAC a reduction in the stroke volume, resulting in a cardiac output decrease, was observed, suggesting that propafenone increases the negative inotropic action of halothane. In dogs anaesthetized with isoflurane 1.2 MAC the decrease in cardiac output was similar to the decrease in heart rate, and therefore no reduction in the stroke volume was observed. The decrease in the heart rate found in this group but not in the halothane group was probably related with the beta-blocker action of the propafenone. Looking to the systemic vascular resistances, our study suggested that propafenone didn't have any vasodilator effect during halogenated anaesthesia.

Anesthesia↗
PubMed1994

Cardiopulmonary effects of halothane in hypovolemic dogs.

Cardiopulmonary effects of halothane administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. Halothane was delivered by face mask, dogs were intubated, then halothane end-tidal concentration of 1.13 +/- 0.02% was maintained, and cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to halothane administration, systemic vascular resistance index, oxygen extraction, and base deficit increased. Compared with baseline values, these variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, pulmonary arterial occlusion pressure, cardiac index, oxygen delivery index, oxygen consumption index, mixed venous oxygen tension, mixed venous oxygen content, venous admixture, arterial bicarbonate concentration, and mixed venous pH. At all times after intubation, arterial and venous oxygen tensions and mixed venous carbon dioxide tensions were increased. Three minutes after intubation, base deficit and mixed venous carbon dioxide tension increased, and mean arterial pressure and arterial and venous pH decreased, compared with values measured immediately prior to halothane administration. Fifteen minutes after intubation, systemic vascular resistance index decreased and, at 15 and 30 minutes, mean arterial pressure and arterial and venous pH remained decreased. At 60 minutes, mean pulmonary arterial pressure and pulmonary arterial occlusion pressure were increased and mixed venous pH was decreased, compared with values measured before halothane administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Anesthetic potency and cardiopulmonary effects of enflurane, halothane, and isoflurane in goats.

Anesthetic requirements, as defined by the minimum alveolar anesthetic concentration (MAC) that prevents gross, purposeful movement in 50% of animals, have not been determined in goats. Therefore, we determined anesthetic potency of enflurane (N = 6), halothane (N = 8), and isoflurane (N = 7) in goats by using the tail clamp and dew-claw clamp as the noxious stimuli and then measured the cardiovascular and respiratory effects of these agents. The MAC was 2.0 +/- 0.4%, 1.3 +/- 0.1%, and 1.5 +/- 0.3% (mean +/- SD) for enflurane, halothane, and isoflurane, respectively. At 1 MAC, when ventilation was changed from controlled to spontaneous, blood pressure decreased in goats anesthetized with isoflurane (98 +/- 17 to 78 +/- 13 mm Hg) and halothane (95 +/- 10 to 83 +/- 14 mm Hg) but did not significantly change in goats anesthetized with enflurane; heart rate increased in goats anesthetized with halothane (117 +/- 12 to 127 +/- 10 beats/min) but was not significantly different in goats anesthetized with enflurane or isoflurane; and cardiac output increased in goats anesthetized with enflurane (5.70 +/- 1.23 to 7.05 +/- 2.02 liters/min) and halothane (6.14 +/- 0.94 to 7.91 +/- 2.45 liters/min) but not with isoflurane. During spontaneous breathing, respiratory depression was manifested by apnea in two animals and an elevated PaCO2: 57 +/- 15 mm Hg, 55 +/- 13 mm Hg, and 59 +/- 14 mm Hg, respectively, for enflurane, halothane, and isoflurane. Minute ventilation during spontaneous breathing was approximately 50% of controlled ventilation for each anesthetic agent.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1994

[The effect of beta-adrenergic blockade on the plasma potassium elevation induced by acute respiratory acidosis during halothane or fentanyl anesthesia].

The effect of beta-adrenergic blockade on the plasma potassium elevation induced by acute respiratory acidosis (CO2 inhalation) was studied in adult mongrel dogs during halothane or fentanyl anesthesia. Twenty-two dogs were divided into 4 groups: halothane-control (HC, n = 15), halothane-beta-blockade (H beta, n = 8), fentanyl-control (FC, n = 15) and fentanyl-beta-blockade (F beta, n = 10). Beta-blockade was achieved by continuous infusion of propranolol. The maximum levels of plasma potassium after 14% CO2 inhalation were 5.0 +/- 0.7 mM (mean +/- SD) in HC, 6.1 +/- 0.8 mM in H beta, 4.3 +/- 0.4 mM in FC and 4.8 +/- 0.5 mM in F beta. With halothane anesthesia more prominent elevation was observed in the beta-blockade group (P < 0.05), but with fentanyl anesthesia this elevation was not significantly different between the two groups. In acute respiratory acidosis, pH-induced plasma potassium elevation is suppressed by simultaneously increased catecholamines, especially epinephrine. Beta-adrenergic blockade, therefore, may cause severe hyperkalemia due to inhibition of adrenergic potassium disposal. During fentanyl anesthesia plasma potassium elevation was less marked than during halothane. This indicates that fentanyl has less suppressing action on the secretion of stress hormones, including epinephrine, under similarly stressful conditions as halothane anesthesia.

Acidosis, Respiratory↗
PubMedDate not supplied

Lipid binding of a halothane metabolite. Relationship to lipid peroxidation in vitro.

Incubation of rat liver microsomes with 14C-halothane in a nitrogen atmosphere results in a high correlation between the formation of conjugated dienes and the binding of a halothane metabolite to phospholipids. Both the binding and the formation of the conjugated dienes required NADPH, were inhibited by carbon monoxide, and increased with duration of incubation and with protein concentration. Both [36Cl] halothane and [14C] halothane showed a similar pattern of binding to microsomal phospholipids suggesting that the chlorine atom is retained by the metabolite that binds. Neither high levels of conjugated dienes produced by halothane in microsomes incubated under nitrogen nor the binding of the halothane metabolite results in the destruction of cytochrome P-450.

Aerobiosis↗
PubMed1993

[Halothane hepatitis].

The greatest disadvantage of the halothane, widely used in the anaesthesiology is its ability to cause liver damage. After halothane anaesthesia mild liver enzyme elevation in the one fifth of the patients was detected. The incidence of fatal halothane hepatitis is rare. It depends on several risk factors: on the genetic predisposition, repeated halothane anaesthetics, female sex, age of patient, obesity, intrahepatic hypoxia and enzyme induction. In the pathophysiology of liver toxicity the metabolism of halothane and immune functions play an important role. In this review the last results of researches concerning to the hepatotoxicity of halothane are summarised and the authors call the attention on the opportunity of its effective prevention.

Anesthesia, Inhalation↗
PubMed1993

Uptake and effects of thiopental in isolated heart preparations of the rat in the presence of halothane.

The uptake of thiopental (CAS 76-75-5) (0.13-0.27 mmol.l-1) into tissue of rat hearts (Langendorff's preparation) was studied in the presence of halothane (CAS 151-67-7). Up to a thiopental concentration of 0.19 mmol.l-1 in the perfusion medium its concentration in heart tissue was significantly increased vs. control when halothane (0.8 vol%) simultaneously was present; using 0.13 mmol.l-1 thiopental and 0.8, 1.5 or 2.0 vol% halothane this increase amounted +12%, +29% and +43%, respectively. Frequency of spontaneously beating rat hearts decreased in the presence of increasing thiopental concentrations. 0.8 vol% halothane (without thiopental) did not influence heart rate; in the presence of thiopental it attenuated heart rate reduction. This attenuation was absent in hearts of rats pretreated with reserpine. 1.5 vol% halothane (itself also without influence on heart rate) increased the negative chronotropic action of thiopental. In isolated right and left atria of rat hearts frequency and contractility decreased concentration-dependently in the presence of thiopental; simultaneously present halothane additionally increased this negative chronotropic and negative inotropic effect of thiopental.

Animals↗
PubMed1996

Cytochrome P450 2E1 is a cell surface autoantigen in halothane hepatitis.

Recent studies have shown that cytochrome P450 2E1 (CYP2E1) is a major catalyst of formation of trifluoroacetylated proteins, which have been implicated as target antigens in the mechanism of halothane hepatitis. In the present investigation, trifluoroacetylated CYP2E1 was detected immunochemically in livers of rats treated with halothane. Furthermore, high levels of autoantibodies that recognized purified rat CYP2E1 but not purified rat CYP3A were detected by enzyme-linked immunosorbent assay in 14 of 20 (70%) sera from patients with halothane hepatitis. Only very low levels of such antibodies were detected in sera from healthy controls, from patients anesthetized with halothane without developing hepatitis, or from patients with other liver diseases. The intracellular distribution of CF3CO-adducts was studied in highly differentiated FGC4 rat hepatoma cell cultures. High levels of adducts were found after 22-hr culture in the presence of halothane, and their generation was dependent on the expression of CYP2E1. Adducts were predominantly located in the endoplasmic reticulum but also, to a minor extent, on the cell surface, as detected by immunofluorescence. A very similar distribution was found for CYP2E1 in FGC4 cells, and immunoprecipitation experiments performed in cultures of FGC4-related Fao hepatoma cells suggest that surface immunoreactivity originates from a small fraction of intact CYP2E1 apoprotein. Human CYP2E1, expressed in V79 cells after cDNA transfection, was also detected to a minor extent in the plasma membrane, whereas no immunofluorescence was evident in parental V79 cells. It is suggested that immune responses to cell surface CYP2E1 could be involved in the pathogenesis of halothane hepatitis.

Animals↗
PubMed1996

Role of L-type calcium channels on halothane-induced myocardial depression in cultured rat ventricular myocytes.

The effects of antagonists for L-type Ca2+ channel, opener and blocker to ATP-sensitive K+ (KATP) channel, phosphodiesterase inhibitor, or Ca2+ sensitizer on halothane-induced myocardial depression were investigated in cultured rat ventricular myocytes. Halothane (1 to 4%) decreased the beating rate and amplitude in a dose-dependent manner. Myocardial depressant effects of halothane were potentiated by the presence of 10 nM nifedipine or verapamil. Neither cromakalim (1 microM), glibenclamide (1 microM), nor pimobendan (10 microM) altered the dose-dependent depressant effects of halothane. The mechanisms involving altered KATP channel, cAMP levels or Ca2+ sensitivity of contractile proteins may not be responsible for myocardial depression during halothane exposure. These results suggest that changes in L-type Ca2+ channel function plays an important role in the volatile anesthetic halothane-induced depression of contractile activity in cultured rat ventricular myocytes.

Anesthetics, Inhalation↗
PubMed1996

Binding of the volatile anesthetic halothane to the hydrophobic core of a tetra-alpha-helix-bundle protein.

Although volatile general anesthetics interact with several proteins, little is known about the location or characteristics of the binding sites at the molecular level. A detailed structural description of how anesthetics associate with macromolecules is necessary for understanding anesthetic mechanisms of action. The recent introduction of designed synthetic proteins provides new opportunities for obtaining structural and functional information on anesthetic-protein interactions. A synthetic tetra-alpha-helix-bundle protein was used to examine the interaction of halothane with a designed protein interior. The tetra-alpha-helix-bundle comprises 124 residues in the form of two identical 62-residue di-alpha-helical peptides, held together in an all-parallel bundle by hydrophobic forces. Steady-state and time-resolved tryptophan fluorescence and circular dichroism spectroscopy were used to study the anesthetic-protein interaction. Halothane quenches bundle tryptophan fluorescence with a dissociation constant of 2.3 +/- 0.4 mM and a Hill number of 0.9 +/- 0.1. Tryptophan fluorescence decay analysis indicates that halothane quenches the protein fluorescence by a static mechanism. Circular dichroism spectroscopy revealed no change in protein secondary structure on exposure to halothane. Dissociation of the tetra-alpha-helix-bundle into 62-residue di-alpha-helical peptides by trifluoroethanol eliminated the halothane-protein interaction. The results suggest that halothane binds to the hydrophobic interior of the tetra-alpha-helix-bundle, close to the tryptophan residues. The protein tertiary and quaternary structures are required for anesthetic binding. This study demonstrates the feasibility of using synthetic tetra-alpha-helix-bundles as model anesthetic-binding proteins. The use of de novo designed bundle proteins should allow structural, energetic and functional descriptions of anesthetic-protein interactions.

Amino Acid Sequence↗
PubMed1996

[Comparative study of recovery from general anesthesia with halothane or sevoflurane in pediatrics].

OBJECTIVES: To assess the clinical signs of awakening and recovery from anesthesia with sevoflurane and 60% nitrous oxide in comparison with halothane and nitrous oxide administered to children. PATIENTS AND METHOD: A prospective study in 39 pediatric ASA I-II patients under 10 years of age scheduled for infraumbilical or otolaryngological surgery. The patients were randomly assigned to 2 groups to receive sevoflurane (n = 20) or halothane (n = 19). All the children received nasal doses of 0.2 mg/kg-1 midazolam before surgery. Induction was achieved by inhalation of a mixture of 40% oxygen and 60% nitrous oxide by face mask along with increasing concentrations of sevoflurane or halothane. Maintenance was with halogenated anesthetic at 1 MAC and 60% nitrous oxide-oxygen along with nerve blockade in the infraumbilical procedures or intravenous analgesia in the otolaryngological operations. We recorded time until awakening, orientation, score on the Aldrete scale and adverse effects during the recovery period. RESULTS: The children who received sevoflurane awoke and were well oriented earlier than were those in the halothane group (10.7 +/- 5.8 versus 18.7 +/- 9.8 min until awakening and 15.4 +/- 8.6 versus 22.1 +/- 10 min for orientation); likewise the sevoflurane group children received higher scores on Aldrete's scale earlier than did those in the halothane group. There were no statistical differences between the 2 groups with respect to side effects during the period of awakening and recovery. CONCLUSIONS: Awakening and recovery are significantly faster with sevoflurane than with halothane, while the incidence of side effects are similar with the 2 agents.

Anesthesia Recovery Period↗
PubMed1997

[Effects of halothane and sevoflurane on reversal of neuromuscular blockade induced by vecuronium in man].

To evaluate residual effects of inhalational anesthetics after reversal of neuromuscular blocking agent, neuromuscular function was monitored after halothane or sevoflurane anesthesia in thirty-seven patients (ASA physical status I or II) for elective surgery after obtaining informed consent. Electromyograph of the adductor pollicis muscle in response to train of four (TOF) stimulation was monitored throughout the study. The first twitch of TOF (T1; % of its control) and the ratio of the fourth twitch to the first twitch of TOF (T4/T1; TR) were recorded at 0, 2, 5, 10, and 15 min after reversal. The patients were divided into five groups; 1) the fentanyl group (n = 7) received fentanyl/N2O; 2) in the halothane stop group (n = 6), halothane was discontinued at least fifteen minutes before neostigmine administration; 3) in the halothane stable group (n = 7), 0.7% halothane was maintained until fifteen minutes after neostigmine; 4) in the sevoflurane stop group (n = 12), sevoflurane was discontinued fifteen minutes before the reversal; 5) in the sevoflurane stable group (n = 5), 3% sevoflurane was maintained until fifteen minutes after the reversal. Anesthesia was induced by thiopental 4 mg.kg-1 and suxamethonium 1 mg.kg-1 and the patients were intubated. After initial dose of vecuronium 0.1 mg.kg-1, the additional dose of 0.02 mg.kg-1 was administered to maintain T1 under 10% of the control value. At the end of the surgery atropine 0.015 mg.kg-1 and neostigmine 0.04 mg.kg-1 were administered to reverse vecuronium when T1 had recovered to 25% of its control. Halothane groups did not differ from fentanyl group. Recovery of T1 at 15 min was suppressed after discontinuation of sevoflurane (86.0 +/- 8.2%) in comparison with fentanyl (97.0 +/- 8.3%). Both T1 (75.4 +/- 12.2%) and TR (68.0 +/- 12.6%) at 15 min after the reversal during 3% sevoflurane inhalation were below those of the stable group. We conclude that the residual sevofulrane after discontinuation of inhalation may impair the neuromuscular transmission after the reversal of neuromuscular blockade. Neuromuscular function should be monitored after the end of anesthesia even though the patient is fully awake.

Adult↗
PubMed1997

[Room air contamination with halothane during pediatric bronchoscopy].

Halothane anesthesia is frequently used for pediatric bronchoscopy. A disadvantage of the equipment used, a rigid bronchoscope together with inhalation anesthesia is the contamination of the working environment. The aim of this study was to determine the exposure of anesthetist and endoscopist during pediatric bronchoscopy under halothane anesthesia in a worst-case working environment and to compare these measurements with the currently valid international threshold values. Ten children (ASA I-III) scheduled for diagnostic bronchoscopy were included in the study. After induction with thiopentone and relaxation with atracurium all children were intubated with a rigid bronchoscope and manually ventilated through a bypass of the bronchoscope. Anesthesia was maintained by means halothane (0.5-2.0 vol%) in 100% oxygen with a flow of 10 l/min. The investigation was done in an operating room without air conditioning and scavenging system. Trace concentrations were measured every 2 minutes in the breathing zones of the anesthetist and the endoscopist by means of a highly sensitive direct reading instrument. Lower detection limit was 0.02 ppm. The mean age (+/- SD) of the children was 29.9 +/- 15.9 months (range: 4 weeks-48 months). Ventilation and oxygenation were stable throughout the bronchoscopic procedure. Mean exposure (+/- SEM) to halothane was 57.7 +/- 18.9 ppm for the anesthetist and 96.3 +/- 22.9 ppm for the endoscopist. The difference was statistically significant (ANOVA, P < 0.05). All international threshold values (2-50 ppm) were exceeded by far. Peak concentrations higher than 200 ppm halothane could be detected several times. The main result of the present study is that under the given situation in the operating room with insufficient room ventilation and no scavenging system halothane anesthesia for rigid bronchoscopy in children results in an occupational exposure that is higher than all known health regulation guidelines. Therefore, in case of insufficient working conditions total intravenous anesthesia might be a better alternative also in very small infants.

Air Pollutants, Occupational↗
PubMed1997

Evaluation of selected cardiopulmonary and cerebral responses during medetomidine, propofol, and halothane anesthesia for laparoscopy in dogs.

OBJECTIVES: To compare the dose-sparing effect of medetomidine on the propofol induction dose and concentration of halothane for maintenance of anesthesia during laparoscopy and to provide guidelines for effective and safe use of these anesthetics in dogs to ensure desirable perioperative analgesia. ANIMALS: 14 purpose-bred dogs. PROCEDURE: Cardiopulmonary and electroencephalographic responses were determined during 2 anesthesia protocols in dogs scheduled for laparoscopy. Fifteen minutes before anesthesia induction, all dogs received atropine sulfate (0.02 mg/kg of body weight, i.m.). Seven dogs were then given propofol (6.6 mg/kg, i.v.); anesthesia was maintained with halothane in oxygen. The other dogs were given medetomidine hydrochloride (10 micrograms/kg, i.m.) 5 minutes after administration of atropine sulfate; anesthesia was then induced by administration of propofol (2.8 mg/kg, i.v.) and was maintained with halothane in oxygen. RESULTS: The halothane concentration required for laparoscopy was lower in dogs given medetomidine. Anesthetic requirements were significantly increased during abdominal manipulation in both groups. Total amplitude of the electroencephalograph in medetomidine-treated dogs was not significantly lower than that in dogs not given medetomidine. Pulmonary responses were stable throughout all procedures. The primary cardiovascular response was an increase in blood pressure associated with the medetomidine-atropine preanesthetic combination. Significant differences in total amplitude or frequency shifts (spectral edge) of brain wave activity were not associated with surgical stimulation. CONCLUSION: Lack of neurologic changes during laparoscopy supports the efficacy of either medetomidine-propofol-halothane or propofol-halothane combinations at higher concentrations to provide desirable analgesia and anesthesia in this group of dogs.

Adrenergic alpha-Agonists↗
PubMed1997

Cytochrome P-4502E1-dependent formation of trifluoroacetyl adducts from halothane by transduced HepG2 cells.

E-9 cells, a HepG2 cell line that has the alcohol-inducible human cytochrome P-4502E1 (CYP2E1) cloned into its genome, was tested for its ability to produce trifluoroacetyl (TFA) adducts from the metabolism of halothane. The metabolism of halothane results in the production of TFA halide that can readily react with cellular proteins to form TFA adducts, which can be detected by antibodies directed against them. E-9 cells formed TFA adducts when incubated with halothane. The major consistent bands that were detected were of molecular weights of approximately 50, 78, and 100 kDa. The formation of these adducts was dependent on halothane concentration and time of incubation with halothane. MV-5 cells, the control cell line that has the viral vector without the P-450, did not produce any adducts. Inhibitors of CYP2E1 function, such as 4-methylpyrazole, inhibited adduct formation. Furthermore, phorbol esters, which have been shown to increase the CYP2E1 level in this cell line, increased TFA adduct formation. This HepG2 cell line may be of value in studying the metabolism and toxicity of halothane in a human cell culture model.

Animals↗