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PubMedDate not supplied

The release of inorganic fluoride from halothane and halothane metabolites by cytochrome P-450, hemin, and hemoglobin.

Halothane (2-bromo-2-chloro-1,1,1-trifluoroethane) releases inorganic fluoride when incubated anaerobically with rat hepatic microsomes reduced with either NADPH or sodium dithionite. Boiled microsomes (cytochrome P-420), hemoglobin, and hemin, each reduced with sodium dithionite, also catalyze the release of inorganic fluoride from halothane, suggesting that the protein portion of cytochrome P-450 is not required for reductive halothane defluorination. 2-Chloro-1,1-difluoroethylene and its bromo analog 2-bromo-1,1-difluoroethylene undergo metabolism in NADPH-reduced microsomes with optimal release of fluoride occurring under air compared to an atmosphere of nitrogen. Neither 2-chloro-1,1,1-trifluoroethane nor 2-bromo-1,1,1-trifluoroethane liberate fluoride in microsomes under air or nitrogen. 2-Chloro-1,1-difluoroethylene and 2-bromo-1,1-difluoroethylene are metabolized predominantly by oxidative cytochrome P-450 metabolism, while reductive pathways utilizing reduced cytochrome P-450, hemoglobin, or hemin liberate fluoride from halothane.

Animals↗
PubMed2000

Expression of steroidogenic enzyme messenger ribonucleic acid and cortisol production in adrenocortical cells isolated from halothane-sensitive and halothane-resistant pigs.

Stress susceptibility in pigs is inherited by a single recessive gene (Hal(n)), and homozygous individuals can be identified by exposure to halothane anesthesia. Previous studies have shown that in stress-susceptible pigs, exposure to a high ambient temperature resulted in a twofold increase in corticotropin (ACTH) and lower plasma cortisol. To determine whether there is a fundamental difference in adrenocortical function between halothane-sensitive (HAL-S) and halothane-resistant (HAL-R) pigs, independent of other factors influencing the hypothalamic-pituitary-adrenal (HPA) axis, we compared cortisol responses to ACTH and 8-bromo-cyclic AMP (8-Br-cAMP) in HAL-S and HAL-R pig adrenocortical cells in vitro. We also determined directly the accumulation of four different mRNAs encoding cholesterol side-chain cleavage cytochrome P450 (P450(scc)), 17alpha-hydroxylase cytochrome P450 (P450(17alpha)), 21-hydroxylase cytochrome P450 (P450(c21)) and 11beta-hydroxylase cytochrome P450 (P450(11beta)) in HAL-S pig adrenal cells and compared them to HAL-R pigs. A time- and dose-dependent increase in medium content of cortisol and cAMP was observed after ACTH treatment. 8-Br-cAMP also caused a time- and dose-dependent increase in cortisol production in the medium. Addition of ACTH or 8-Br-cAMP to HAL-S and HAL-R male Lanyu small-ear miniature pig adrenocortical cells increased cortisol production in a dose- and time-related manner. However, cells isolated from HAL-S pigs had a lower cortisol production in response to ACTH or 8-Br-cAMP compared to those from HAL-R pigs. Treatment of cultured cells with 8-Br-cAMP (0.5 mM) for 18 h resulted in a significant increase in P450(scc), P450(17alpha), P450(c21), and P450(11beta) mRNA levels. In the absence of 8-Br-cAMP, the four genes were expressed constitutively in both HAL-S and HAL-R pig adrenal cells. Densitometric scanning of the autoradiograph indicated that the relative amounts of P450(scc) and P450(17(alpha)) mRNAs in HAL-S pig adrenal cells were between 48% and 53% of those detected in HAL-R pig adrenal cells (P < 0.05). No difference in the amounts of P450(c21) and P450(11beta) was seen in HAL-S and HAL-R pig adrenal cells. Addition of 8-Br-cAMP (0.5 mM) resulted in a uniform increase in the levels of all four P450 mRNAs in both HAL-S and HAL-R pig adrenal cells. However, the amounts of P450(scc) mRNA in HAL-S pig adrenal cells were 67% (P < 0.05) of those measured in HAL-R pig adrenal cells, whereas the amounts of P450(17alpha ), P450(c21), and P450(11beta) mRNAs were similar in these cells. Our data suggest an HPA axis defect in HAL-S pigs at the adrenal level. This defect appears to be at the level of P450scc gene expression, which could be partially related to reduced cortisol production by ACTH stimulation.

Adrenal Cortex↗
PubMed1986

The interaction of enflurane, halothane and the halothane metabolite trifluoroacetic acid with the binding of acidic drugs to human serum albumin. An in vitro study.

The interaction of the volatile anaesthetics enflurane, halothane and the halothane metabolite trifluoroacetic acid with the binding of two highly bound acidic drugs (warfarin, phenytoin) to albumin has been studied in vitro by equilibrium dialysis. Trifluoroacetic acid (TFA) inhibited the binding of both drugs to human serum albumin (HSA). Halothane, on the other hand, increased the binding of warfarin to HSA, while enflurane inhibited only the binding of phenytoin. It seems that the binding of the acidic drugs warfarin and phenytoin to HSA is more sensitive to the structures of the gases than for the basic drug diazepam which was previously shown to be equally affected by both gases. Furthermore, it seems that drugs competing for the same binding site (warfarin, phenytoin) may respond differently to conformational changes of the site. It is suggested that drugs bound to the "diazepam site" are more easily affected by the volatile anaesthetics than drugs bound to the "warfarin site".

Binding Sites↗
PubMed1994

Recovery after propofol infusion anaesthesia in children: comparison with propofol, thiopentone or halothane induction followed by halothane maintenance.

We have compared the recovery profiles of 163 healthy Chinese children after general anaesthesia for minor surgical procedures. Patients were allocated randomly to receive one of four anaesthetic techniques: propofol infusion for induction and maintenance using a pharmacokinetic model-controlled syringe pump set initially at a target concentration of 8 micrograms ml-1 and then adjusted according to clinical requirements; propofol 2.5-3.5 mg kg-1, thiopentone 4-5 mg kg-1 or 2-3% halothane for induction of anaesthesia followed by 1-2% halothane for maintenance of anaesthesia. All patients breathed a mixture of 70% nitrous oxide in oxygen through a laryngeal mask airway and received an appropriate regional anaesthetic block. Recovery was assessed using the time to achieve full Steward score, open eyes on command, orientation and the time required to complete a simple puzzle. Recovery was slowest with the propofol infusion (mean 39.8 (SD 12.9) min when eyes opened on command). The recovery times were significantly shorter with the three other techniques (propofol bolus 21.9 (9.9) min, thiopentone 23.4 (11.3) min, halothane 20.1 (8.9) min), and the choice among these three methods had no significant influence on the recovery profile.

Anesthesia Recovery Period↗
PubMed1984

General anaesthesia with halothane and drug absorption. The effect of general anaesthesia with halothane and diazepam on postoperative gastric emptying in man.

The effect of general anaesthesia with halothane on postoperative absorption of paracetamol was measured in seven patients, after minor surgery on the extremities. Gastric emptying, estimated indirectly by the rise in serum paracetamol following oral administration of the drug, was significantly delayed after general anaesthesia with halothane compared with gastric emptying when general anaesthesia with halothane was not administered. It was furthermore demonstrated that absorption of paracetamol and therefore gastric emptying were normal or nearly normal when diazepam 15 mg was given orally to the same patients 2 weeks later.

Acetaminophen↗
PubMedDate not supplied

Failure to induce hepatic pathology in animals sensitized to a halothane metabolite and subsequently challenged with halothane.

The results of this animal study confirm the induction of delayed hypersensitivity to a halothane metabolite, but the sensitization does not cause hepatic damage on subsequent halothane exposures. Before the hypothesis that hepatic necrosis following halothane has an immunologic basis can be accepted or rejected, more critical studies with different approaches must be made.

Animals↗
PubMed1989

The pathology of halothane hepatotoxicity in a guinea-pig model: a comparison with human halothane hepatitis.

The pathology of halothane hepatotoxicity is described in detail in a guinea-pig model. Twenty-two of 40 guinea-pigs developed liver damage after exposure to 1% halothane in 21% O2 for 4 h. The other 18 animals showed no evidence of hepatic injury. Two distinct patterns of damage were identified: mild damage, in which livers had focal areas of necrosis, and severe damage, where necrosis was confluent around the terminal hepatic venules, often extending to the portal tracts. Serum alanine aminotransferase activity was significantly elevated in guinea-pigs with severe liver damage. Hepatocytes in the damaged areas showed degenerative changes ranging from vacuolization to ballooning degeneration and necrosis. Inflammatory cells, predominantly lymphocytes, were often present in the areas of necrosis. The pathology of mild and severe liver injury in the guinea-pig closely resembles the spectrum of injury observed in non-fatal halothane hepatitis in man.

Alanine Transaminase↗
PubMed1985

[Centrolobular liver cell necroses following occupational halothane contact. Association with antibodies to halothane altered liver cell components].

A report is given on a 24 year old nurse, who developed two episodes of fever, chills and malaise with high serum enzyme levels and histologic proof of extensive centrolobular hepatic necrosis in association with vocational halothane exposure in the operating theatre. A cause-effect relationship was suggested by the demonstration of antibodies against halothane-altered hepatocyte membrane components. Also, there was no indication of other known causes of a cytotoxic liver reaction. In certain predisposed individuals, halothane even in subanaesthetic concentrations is apparently able to induce liver cell damage. Only six further reports on such liver injuries in medical personnel could be found in the literature.

Adult↗
PubMed1993

[The clastogenic effect of halothane on the lymphocytes from patients operated on under halothane anesthesia].

The clastogenic effect of halothane anesthesia on peripheral blood lymphocytes from operated patients was studied. Chromosomal aberrations and sister chromatic exchanges in lymphocyte cultures of 7 patients were analyzed. Blood samples were obtained before the operative intervention, immediately after the effect of anesthesia was over and 24 hours later. To differentiate sister chromatids in the culture medium, on the 24th cultivation hour bromodeoxyuridine in final concentration 10 micrograms/ml was added. Increased incidence of structural chromosomal aberrations was recorded in lymphocyte cultures of patients after anesthesia--6.43 per cent cells with aberrations in the first post-halothane culture and 8.28 per cent in the second. Comparison of the cell affection index with the total number of affected cells revealed a continuous clastogenic effect pattern within the study period. Reliable evidence for induction of sister chromatid exchanges after the anesthesia was not found. The results were debated in the light of the possible mechanisms of clastogenicity of halothane anesthesia, the initial state of the patients and the consequences for them.

Adult↗
PubMed1976

Elevation of plasma bromide levels in patients following halothane anesthesia: Time correlation with total halothane dosage.

Plasma bromide concentrations of 25 patients were determined before and after halothane anesthesia. A high correlation (r greater than .70) between exposure to halothane in MAC-hours and plasma bromide levels 24, 48 and 72 hours later was found. Peak bromide levels occurred 48-72 hours after anesthesia in 16 patients (64 per cent), and ranged from 52 mug/ml (0.65 mEq/l) to 180 mug/mo (2.25 mEq/l). Bromide levels remained elevated for prolonged periods (at least 22 days in some patients). Possible sedative or psychoactive effects of increased plasma bromide levels are discussed.

Bromides↗
PubMed1977

Glomerular filtration rate during halothane anaesthesia and epidural analgesia in combination with halothane anaesthesia.

Pre- and peroperative determination of glomerular filtration rate (GFR) was performed in nine patients operated during light halothane anaesthesia (group A) and in nine patients operated during epidural analgesia in combination with light halothane anaesthesia (group B). In group A, the mean GFR decreased insignificantly by 7% and the mean arterial blood pressure increased significantly by 10%. In group B, the mean GFR decreased significantly by 19% and the mean arterial blood pressure decreased significantly by 15%. It is suggested that the difference in change in GFR between the two groups was caused by differences in mean arterial blood pressure.

Adult↗
PubMed1992

Evaluation of greyhound susceptibility to malignant hyperthermia using halothane-succinylcholine anesthesia and caffeine-halothane muscle contractures.

We investigated Greyhounds because of prior reports of malignant hyperthermia (MH) episodes and because Greyhounds may express high genetic relatedness due to inbreeding for generations. Seven Greyhound and six mongrel dogs were given halothane and succinylcholine anesthesia as a challenge to trigger MH. They also underwent semitendinosus muscle biopsy for contracture study with halothane and caffeine. Measurements in vivo of mixed venous and arterial blood gases, cardiac output by thermodilution, temperature, blood pressure, and pulse rate provided sequential data regarding whole body O2 consumption (product of cardiac output and arterial-mixed venous O2 content difference), acid-base status, and arterial CO2 tension. Greyhounds and mongrels had uniformly similar in vivo and in vitro responses, without evidence for MH. Contracture thresholds were higher than those reported for normal swine and humans (8 mM vs. 4 mM). Information on MH susceptibility in this breed is important for laboratory investigation in Greyhounds as well as to veterinary medicine in general. Neither mongrels nor this group of Greyhounds were obviously susceptible to MH. If all Greyhounds are genetically homologous, then Greyhounds may not be specifically MH susceptible. These findings overall may provide a protocol and baseline normal comparative data for determining MH susceptibility in dogs and other species.

Anesthesia, Inhalation↗
PubMed1976

Effect of halothane and halothane-nitrous oxide on hematocrit and plasma protein concentration in dog and monkey.

Hematocrit and plasma protein concentration in healthy dogs and monkeys (Macaca arctoides) awake and anesthetized with halothane-oxygen and halothane-nitrous oxide oxygen were compared during conditions of spontaneous and controlled ventilation. Both hematocrit and plasma protein concentration decreased within 15 minutes following anesthetic induction. This decrease persisted throughout constant- or variable-depth anesthesia and did not vary appreciably with ventilation, anesthetic dose, or introduction of nitrous oxide. Plasma volume, determined by a dye dilution technique, concomitantly increased. This increase is compatible with the directional changes in hematocrit and plasma protein.

Anesthesia, Inhalation↗
PubMed1988

Anaesthetic induction with isoflurane or halothane. Oxygen saturation during induction with isoflurane or halothane in unpremedicated children.

The authors performed a randomised, prospective trial in which one junior anaesthetist administered gaseous induction of anaesthesia to 50 unpremedicated children with either isoflurane or halothane in nitrous oxide and oxygen. Arterial oxygen saturation and the electrocardiogram were monitored and the incidence of complications noted. Desaturation below 85% occurred in six children, but only with isoflurane. The incidences of complications and desaturation events did not alter throughout the 25 isoflurane inductions. Coughing, movement, laryngospasm and sinus tachycardia occurred more frequently with isoflurane. Isoflurane inductions took longer (7.9 as compared with 5.4 minutes, p less than 0.001) and had 4.25 times the number of complications.

Anesthesia, Inhalation↗
PubMed1982

The effects of halothane-and-oxygen anesthesia, and of halothane-nitrous oxide-and-oxygen anesthesia on tympanograms in the dog.

Electroacoustic tympanograms were recorded from both ears of 20 dogs of either sex, aged 6 mo to 12 yrs, prior to anesthesia, at 10 min after halothane- and-oxygen (HO) anesthesia, and at 5 min after nitrous oxide was added to the HO mixture (HNO). Both HO and HNO anesthesia significantly increased compliance and peak pressure values from pre-anesthetic (own control) values. In addition, HNO anesthesia significantly increased peak pressure values above HO anesthesia levels. HNO compliance values were not significantly different from HO values. These results suggest that tympanograms recorded during either HO or HNO anesthesia in the dog will be altered and that interpretation of the tympanograms should include consideration of the state of consciousness of the animal during recording.

Acoustic Impedance Tests↗