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PubMed1983

Local cerebral glucose consumption in the rat. II. Effects of unilateral substantia nigra stimulation in conscious and in halothane-anesthetized animals.

The energy metabolism of 74 anatomically discrete central nervous structures was investigated by means of the autoradiographic 2-deoxy-D-(1-14C)glucose method (14C-DG) in conscious awake, as well as in halothane-anesthetized rats, following unilateral substantia nigra (SN) electrical stimulation. All the basal ganglia structures displayed bilateral metabolic activation in conscious animals, with only the contralateral subthalamic nucleus being unaffected. In anesthetized rats only the SN reticulata, globus pallidus, and subthalamic nucleus were affected ipsilaterally whereas anesthesia masked the effects of SN stimulation in SN compacta and striatum ipsilaterally, as well as within all the above structures contralaterally. The entopeduncular nucleus was bilaterally activated no matter the state of consciousness. Unilateral SN stimulation also increased glucose utilization within several thalamic regions (ventromedial, ventrolateral, ventroanterior, intralaminar, ventrobasal, and mediodorsal nuclei), the habenular complex, a few mesencephalic, brainstem (locus coeruleus and dorsal raphe) and cerebellar structures, mostly bilaterally and independently of the state of consciousness. Some of the factors suggested to be responsible for the masking effects of halothane-anesthesia on the metabolic activations elicited by unilateral SN stimulation are the following: (1) absence of movements in anesthetized rats, (2) halothane-induced depression of polysynaptic pathways mostly mediated through the thalamus, and (3) the stimulatory effect of halothane-anesthesia itself on metabolic activity in both parts of the SN.

Anesthesia, General↗
PubMed1991

Effect of calcium channel blocking agents on the reductive metabolism of halothane.

The effect of calcium channel blocking agents on the reductive metabolism of halothane in liver microsomes of guinea pigs was investigated. The reaction mixture for the measurement of the end products consisted of microsomal suspension, 5 mM NADPH, calcium channel blocking agents (verapamil, diltiazem, nicardipine and nifedipine) and halothane in 0.1 M phosphate buffer (pH 7.4). The reductive metabolism of halothane was inhibited competitively by verapamil, diltiazem and nicardipine. The binding spectra for the interaction of these three drugs with cytochrome P-450 in microsomes were investigated. Verapamil caused the reverse type I difference spectrum and diltiazem caused the type I difference spectrum. However, the change caused by nicardipine was not observed by the presence of its specific spectra. NADPH-cytochrome P-450 reductase activity in microsomes did not change by the addition of these three drugs. These results suggest that these three calcium channel blocking agents inhibit the production of radical intermediates during the reductive metabolism of halothane.

Animals↗
PubMedDate not supplied

Inhibitory effect of gomisi on reductive metabolism of halothane.

The effect of Gomisi (dried ripe fruit of schizandra chinensis) on chlorodifluoroethylene (CDE) and chlorotrifluoroethane (CTE) formation was investigated. The incubation mixtures for the measurement of reductive metabolites of halothane consisted of liver microsomal suspensions, 3 mM NADPH, extract solution of Gomisi and halothane in 0.1 M potassium phosphate buffer (pH 7.4). The production of CDE and CTE was inhibited by Gomisi in a dose-dependent way. The production were reduced to half in the presence of 0.5% Gomisi extract in the reaction mixture. The results suggest that Gomisi can inhibit the reductive metabolism of halothane in vitro; thus it may protect against halothane-induced hepatitis.

Animals↗
PubMed1980

Suppressive effects of thiopental and halothane on specific arms of the immune response.

The effect of thiopental, halothane and surgery on specific arms of the immune response of normal mice was studied. These experiments represent the first step in localizing a potentially correctable anesthesia/surgery-induced defect in immune reactivity which may be involved with postoperative increases in tumor growth. The delayed-type hypersensitivity (DTH) response of mice to 2,4-dinitrochlorobenzene (DNCB) was studied. Combinations of induction and inhalation anesthesia and surgery were administered at various phases of the immune response to DNCB. Thiopental impaired the afferent response while halothane impaired the efferent response. When the agents were combined, both arms of the immune response were suppressed. A surgical procedure, in most experiments, did not produce a greater immunosuppression than thiopental and halothane. The administration of an immunorestorative agent, thiabendazole, returned reactivity to normal levels. Thiopental and halothane either affect different immune cell populations or they affect different functions of a cell population active in both arms of the DTH response. In relation to tumor growth, the degree of suppression may not be as significant as the cell population impaired.

Anesthesia↗
PubMed1989

Determination of halothane distribution in the rat head using 19F NMR technique.

The distribution of halothane in the rat head was examined with 19F NMR rotating-frame zuegmatography and 2DFT 19F NMR imaging. The rotating frame experiments were conducted at varying times following anesthesia to assess the time dependence of the halothane distribution. The results of these experiments demonstrate that halothane and halothane metabolite are unequally partitioned through the rat tissues examined. 19F spin-echo imaging experiments were conducted immediately following anesthesia. The results of these experiments are compared with those of the spectroscopic technique.

Anesthesia, Inhalation↗
PubMed1993

In vivo fluorine-19 magnetic resonance spectroscopy of cerebral halothane in postoperative patients: preliminary results.

This study reports the use of 19F MRS to study halothane in the brain of eight patients recovering from halothane anesthesia of short duration. Resonances attributable to halothane were observed up to 90 min after withdrawal of the anesthetic agent. The signal-to-noise ratio for an unlocalized spectrum acquired using a 6 cm surface coil was typically 20 with data collection times of 2 min. In seven patients a single resonance was seen with a mean (+/- SD) chemical shift of +43.3 (+/- 1.8) ppm, referenced to NaF at 0 ppm. This resonance exhibited a T1 value of between 0.5 and 1 s, and a T2* (estimated from the linewidth of the resonance) between 3.5 and 10 ms. In one patient two resonances were observed with chemical shifts of +38 and +41 ppm. Because we cannot exclude the possibility that this was due to field inhomogeneity, the significance of the last finding is uncertain. However, phantom studies show that the chemical shift of halothane in different environments (such as water, olive oil, methanol, and lecithin) can vary to an extent that accounts for the two resonances seen in our patient. These results demonstrate the feasibility of in vivo 19F MRS studies of fluorinated volatile agents in humans. The potential for clinical 19F MRS of fluorinated anesthetics is discussed.

Adult↗
PubMed1988

Halothane prevents nitrous oxide teratogenicity in Sprague-Dawley rats; folinic acid does not.

The teratogenic effects of nitrous oxide (N2O) administered with halothane or folinic acid (FA) were studied in two separate experiments using a total of 206 timed-pregnant Sprague-Dawley rats. In each experiment, rats were exposed to either 1) air (n = 30-40); 2) N2O (50-75% for 24 h on day 8 of pregnancy, n = 20-30); 3) test agent (i.e., 0.27% halothane for 24 h on day 8 of pregnancy; or 5 mg/kg/day of FA on day 5-13 of pregnancy, subcutaneously by osmotic pump, n = 20-30); or 4) N2O + test agent (n = 20-30). Cesarean sections were performed on day 20, and fetuses were examined for visceral and skeletal abnormalities. There were no differences in pregnancy rate, number of implantations and live fetuses per rat, and fetal weight among any of the groups. Treatment with N2O resulted in significantly higher incidences of resorptions and of major visceral and minor skeletal abnormalities. Halothane administered with N2O protected against these effects; folinic acid did not. Using an additional 65 nonpregnant rats, hepatic methionine synthase activity was measured after treatment with 50% N2O, 50% N2O plus 0.27% halothane, or 50% N2O plus 5 mg/kg/day of folinic acid. Methionine synthase activity was equally depressed in all groups. These findings do not support the commonly held theory that inactivation of methionine synthase is the sole cause of N2O teratogenicity; rather, they suggest a multifactorial etiology, which may include changes in uterine blood flow.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed2000

Effects of halothane, enflurane, and isoflurane on measurements of Ca(2+) by calcium electrode and aequorin luminescence.

We assessed the possible effects of the volatile halogenated anesthetics halothane, enflurane, and isoflurane on Ca(2+) electrode measurements and on the Ca(2+) sensitivity of the bioluminescent protein aequorin. In Ca(2+)-EGTA buffers of different pCa values (7. 870, 6.726, 6.033, 4.974, 4.038, and 2.995) and in serial Ca(2+) dilutions (10(-4), 10(-3), and 10(-2) M), halothane, enflurane, and isoflurane each caused a concentration-dependent and reversible increase in the absolute value of the negative electrode potential. Isoflurane and enflurane had larger effects than halothane. Neither of these anesthetics changed aequorin luminescence at any pCa tested in the range 2-8. There was no potentiation or inactivation of aequorin luminescence over a period of up to 2 h. These results suggest that (1) halothane, enflurane, and isoflurane interfere with Ca(2+) electrode measurements, most likely by changing the physicochemical properties of the membrane; (2) these anesthetics do not inactivate or otherwise modify the characteristics of the reaction of Ca(2+) with aequorin; and (3) these anesthetics do not change the apparent affinity of EGTA for Ca(2+).

Aequorin↗
PubMed1991

Halothane-induced membrane reorganization monitored by DSC, freeze fracture electron microscopy and 31P-NMR techniques.

The effect of the volatile anaesthetic halothane on the structure and dynamics of lipid multilayers (dimyristoyl- and dipalmitoylphosphatidylcholine, DM- and DP-PC, aqueous dispersions) was studied using Differential Scanning Calorimetry (DSC), Freeze Fracture Electron Microscopy and solid state phosphorus-31 Nuclear Magnetic Resonance (31P-NMR). The action of the drug depends upon the halothane-to-lipid molar ratio, Ri, and temperature. With DPPC lipids, three main regions can be distinguished: i) 0 less than Ri less than 0.7, ii) 0.7 less than Ri less than 2 and iii) Ri greater than 2. As Ri increases in the first region, a linear decrease in the main gel-to-fluid phase transition temperature (Tc), a broadening in the DSC transition peak and a lowering in the enthalpy variation (delta H), are observed. A minimum in delta H is reached at Ri = 0.7. In this region, 31P-NMR spectra indicate that the multibilayer structure is maintained. In the second region, Tc still decreases with the same slope, but delta H increases up to a plateau value for Ri = 2. In the lipid fluid phase, an isotropic NMR line appears superimposed on the powder pattern that corresponds to a lamellar phase. For Ri greater than 2, Tc and delta H remain almost constant. At values of temperature that are greater than Tc, a growing isotropic line occurs in 31P-NMR spectra. This means a new supramolecular structure made of lipids and halothane is stabilized. This structure has been characterized as small vesicles of about 400 A to 600 A diameter by Freeze Fracture electron microscopy observations. With DMPC and low ratios (Ri less than or equal to 2), DSC and NMR results are similar to those obtained for DPPC. However, the minimum delta H is reached at Ri = 0.2 and the decrease in Tc is faster than for DPPC when Ri increases from 0. For Ri greater than 2, while Tc and delta H remain constant as in the case of DPPC, 31P-NMR spectra of DMPC systems show a superimposition of an isotropic line and two powder patterns, which correspond to small tumbling vesicles, a possible hexagonal phase and a lamellar phase respectively. Halothane, thus acts on model membranes in two different steps: at low Ri the bilayer is disturbed but keeps its structure. Whereas for higher drug concentrations, a new organization of lipids seems to be stabilized for T greater than Tc.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1979

Effects of halothane on microtubules in the sciatic nerve of the rat.

The effect of halothane and colchicine on microtubule repolymerisation after exposure to cold has been examined in the sciatic nerve of the rat. Myelinated axons showed a significant decrease in microtubule numbers and density after exposure to both 20 mM halothane and 10(-5) M colchicine; exposure to both agents simultaneously produced a further significant reduction when compared to halothane alone. It is suggested that halothane can interfere with microtubule repolymerisation in mammalian axons possibly in a similar way to that described in invertebrates.

Animals↗
PubMed1975

A comparative study on the irreversible binding of labeled halothane trichlorofluoromethane, chloroform, and carbon tetrachloride to hepatic protein and lipids in vitro and in vivo.

1) After intraperitoneal injection of labeled CCl4, CHCl3, and halothane in mice, 14C is preferentially bound to liver endoplasmic protein and lipid. A considerable activity is also associated with mitochondrial constituents. Maximal protein binding (nmol/mg): CCl4: 2.8 (0.5 hrs); CHCl3: 11.5 (6 hrs); halothane: 5 (6 hrs). Lipid binding: CCl4: 6.4 (5 min); CHCl3: 8 (4 hrs); halothane: 13.5 (2 hrs). The form of the binding curves in microsomal and mitochondrial protein and lipid differed with the individual haloalkanes. 2) The irreversible (covalent) binding of 14C from labeled haloalkanes in anaerobic suspensions of isolated rabbit liver microsomes and NADPH after 30 min was for protein (lipid) (nmol/mg): CCl4: 15 (58); CHCl3: 3.4 (3.2); halothane: 2.3 (10); trichlorofluoromethane: 6.5 (30). Anerobic incubation favored dehalogenation, but CHCl3 metabolism and irreversible binding requires oxygen. The greatest differences in the in vitro "covalent" binding rates were observed with CHCl3 in rat, mouse, and rabbit. 3) Altered microsomal cytochrome P-450 concentrations in newborn animals, or produced by pretreatment of rats with phenobarbital, 3-methylcholanthrene (MC), or CoCl2 effected similar, but not proportional changes in the rates of irreversible protein and lipid binding. Upon addition of CCl4 the difference of light absorption of reduced liver microsomes from MC-pretreated rats containing cytochrome P-448 appeared at 452 nm. The irreversible binding rate in these microsomes was also increased. The small accleration in irreversible binding in liver microsomes from rats pretreated with isopropanol is not proportional to the high increase of CCl4 toxicity. 4) Practically no binding to added, soluble albumin or RNA was observed in microsomal incubates. However, 14C is bound to the nicotine-adenine dinucleotides of the NADPH system. All haloalkanes produced a similar increase of NADPH oxidation in incubates of rabbit liver microsomes and NADPH.

1-Propanol↗
PubMed1982

Effect of halothane anesthesia on end-tidal PCO and pattern of respiration in the rat.

End-tidal Pco2 (petco2) and ventilation of the rat anesthetized with halothane were measured. The Petco2 measured by an infrared analyzer agreed well with the simultaneously measured Paco2 in the range from 20-60mm Hg (2.7-8.0 kPa). When the level of anesthesia was deepened by increasing the halothane concentration from 0.9-3.0%, minute ventilation was decreased progressively accompanied by a rise in Petco2 and the CO2 output was reduced. Halothane induced a progressive decrease in frequency of respiration (f) with almost constant or even slight increase in tidal volume (VT)). Decrease in f was caused largely by the prolongation of expiratory duration (TE). Changes in inspiratory duration (T1) were small and the mean VT/T1 ratio remained unaltered at different levels of anesthesia. These changes in respiratory pattern induced by halothane anesthesia contrasted with the simultaneous decrease in VT, f and VT/T1 ratio and apparent changes of both T1 an TE reported in other species. Species differences in effects of anesthesia on ventilation were discussed. Restraining the rat on a stereotaxic apparatus with head holders, especially with ear bars, elicited an initial transient stimulation of ventilation which was followed by a strong depression.

Anesthesia, General↗
PubMed1989

Inhibition by halothane, but not by isoflurane, of oxidative response to opsonized zymosan in whole blood.

In an attempt to clarify some apparent discrepancies in reports of the effects of anesthetic agents upon granulocyte function, we studied the effects of halothane and isoflurane, using techniques that allowed us to perform the assays in and in sealed vials to prevent volatile gas evolution: assay gas concentrations were measured, rather than inferred. Chemiluminescence, superoxide production, and hydrogen peroxide production were assessed after presentation of opsonized zymosan as a phagocytic stimulus. Incubation with halothane led to a highly statistically significant dose-related inhibition of chemiluminescence (maximum 66%), H2O2 production (67%) and .O2- production (61%), within the concentration range observed in blood from patients undergoing general anesthesia. In contrast, the presence of isoflurane led to no statistically significant changes in any of the functions measured. Cells harvested from patients undergoing elective halothane anesthesia showed the same functional inhibition, but for quantitative differences likely due to the inability to control for dilution effects in clinical samples. It has been suggested that halothane anesthesia may be associated with excess mortality in septic patients; although the results we report are readily reversible, their presence during a prolonged anesthesia could be harmful in a patient who is not immunologically normal and/or who is already infected. Careful clinical trials will be necessary to determine if isoflurane is a superior agent in this context.

Blood↗
PubMed1991

Effects of the anesthetics heptanol, halothane and isoflurane on gap junction conductance in crayfish septate axons: a calcium- and hydrogen-independent phenomenon potentiated by caffeine and theophylline, and inhibited by 4-aminopyridine.

This study has monitored junctional and nonjunctional resistance, [Ca2+]i and [H+]i, and the effects of various drugs in crayfish septate axons exposed to neutral anesthetics. The uncoupling efficiency of heptanol and halothane is significantly potentiated by caffeine and theophylline. The modest uncoupling effects of isoflurane, described here for the first time, are also enhanced by caffeine. Heptanol causes a decrease in [Ca2+]i and [H+]i both in the presence and absence of either caffeine or theophylline. A similar but transient effect on [Ca2+]i is observed with halothane. 4-Aminopyridine strongly inhibits the uncoupling effects of heptanol. The observed decrease in [Ca2+]i with heptanol and halothane and negative results obtained with different [Ca2+]o, (Ca2+)-channel blockers (nisoldipine and Cd2+) and ryanodine speak against a Ca2+ participation. Negative results obtained with 3-isobutyl-1-methylxanthine, forskolin, CPT-cAMP, 8Br-cGMP, adenosine, phorbol ester and H7, superfused in the presence and absence of caffeine and/or heptanol, indicate that neither the heptanol effects nor their potentiation by caffeine are mediated by cyclic nucleotides, adenosine receptors and kinase C. The data suggest a direct effect of anesthetics, possibly involving both polar and hydrophobic interactions with channel proteins. Xanthines and 4-aminopyridine may participate by influencing polar interactions. The potentiating effect of xanthines on cell-to-cell uncoupling by anesthetics may provide some clues on the nature of cardiac arrhythmias in patients treated with theophylline during halothane anesthesia.

4-Aminopyridine↗
PubMed1980

Brain cyclic nucleotide and energy metabolite responses to subanesthetic and anesthetic concentrations of halothane.

Adult rats were exposed to 0.5, 1.0 and 1.5% halothane, delivered in air, for 1 h. Whole brain 3',5'-cyclic adenosine monophosphate (cAMP) of halothane-exposed rats showed only a slight increase relative to control values. 3',5'-Cyclic guanosine monophosphate (cGMP) was increased significantly in halothane-exposed rats, and the response was directly related to the halothane concentrations. Adenosine triphosphate (ATP) and phosphocreatine (PC) remained unchanged relative to control values. Correspondence of these values to apparent discrepancies in the literature is discussed.

Adenosine Triphosphate↗
PubMed1993

The effect of diclofenac and ketoprofen on halothane MAC in rabbit.

Non-steroidal anti-inflammatory drugs obviously act also on the central nervous system. We, therefore, studied the effect of diclofenac 3 mg/kg and ketoprofen 4 mg/kg on the minimum alveolar concentration (MAC) of halothane in 10 New Zealand White rabbits. After determination of halothane MAC, total doses of NSAIDs were administered intravenously as three subdoses: 12.5%, 37.5% and 50% of the total dose. Depth of anaesthesia did not increase significantly after the first two doses with either drug. With ketoprofen, halothane MAC increased after subdose 3 from 1.52 (SD 0.42) vol% to 1.9 (SD 0.36) vol% (p < 0.01). With diclofenac, halothane MAC increased after subdose 3 from 1.44 (SD 0.18) vol% to 1.60 (SD 0.39) vol% (ns). With both drugs, large interindividual differences of MAC appeared after full doses of NSAIDs.

Anesthesia, Inhalation↗
PubMed1975

Doses of epinephrine causing arrhythmia during enflurane, methoxyflurane and halothane anaesthesia in dogs.

The arrhythmogenic dosage of epinephrine, administered by constant intravenous infusion, was measured in five dogs during enflurane, methoxyflurane and halothane anaesthesia. While premature ventricular contractions were observed in only one of five dogs with enflurane and methoxyflurane, epinephrine-induced arrhythmias were seen in all animals during halothane anaesthesia. Epinephrine dosage and the resultant increase in mean arterial blood pressure at which arrhythmias occurred during halothane anaesthesia were significantly less (p less than 0.05) than with the other anaesthetics. These observations indicate that enflurane and methoxyflurane, as compared to halothane, possess relatively less arrhythmogenic potential as sensitizing agents in the presence of increased circulating catecholamines.

Anesthesia, Inhalation↗
PubMed1976

The effects of furosemide on remal blood flow and cortical perfusion during methoxyflurane and halothane anaesthesia.

Nephrotoxicity due to methoxyflurane may be due in part to alterations in intra-renal perfusion. Furosemide is believed to alter the intra-renal distribution of blood flow. Studies have been carried out to observe the effects of systemic furosemide administration during methoxyflurane and halothane anaesthesia in normotensive animals and in animals made hypotensive by increasing inspired concentrations of the anaesthetics. During halothane anaesthesia normotensive dogs showed a rise in total renal blood flow during the infusion of furosemide. Hypotensive dogs showed no increase in flow. During methoxyflurane anaesthesia no change in total renal blood flow followed furosemide administration to normotensive animals. Some diminution in total blood flow followed the administration of furosemide in hypotensive dogs during methoxyflurane anaesthesia. In normotensive dogs during halothane anaesthesia there was a significant increase in deep cortical perfusion after furosemide. Furosemide, therefore, is unlikely to mitigate the potential for nephrotoxicity which methoxyflurane possesses. Furthermore, this diuretic may adversely influence renal function when administered during halothane anaesthesia.

Anesthesia, Inhalation↗