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PubMed1996

Halothane acts as a partial agonist of the alpha6 beta2 gamma2S GABA(A)receptor.

Whole-cell patch clamp recording was performed on human embryonic kidney 293 cells stably transfected with rat cDNAs for the alpha6, beta2, and gamma2S subunits of the GABA(A) receptor. The volatile anesthetic halothane directly activated a current in the absence of the ligand gamma-aminobutyric acid (GABA). Both the current amplitude and the rate of desensitization increased in a dose-dependent manner with an EC50 of 1.0+/-0.2 mM and a Hill coefficient (nh) of 1.5+/-0.1. The EC50 and nh for GABA to activate the receptor were 1.0+/-0.3 microM and 1.4+/-0.2, respectively. The peak amplitude of the halothane-activated current was about 4% of the maximal GABA response, which was not changed when the concentration of Ca2+ in the external solution was decreased from 2 mM to 0.2 mM. The reversal potential of both halothane- and GABA-activated currents changed with the external Cl- concentration as predicted by the Nernst equation for chloride ions. The halothane- and GABA-activated currents were blocked by both the noncompetitive GABA(A) receptor antagonist picrotoxin and the competitive GABA(A) receptor antagonist bicuculline. Schild plots revealed that the K(i)s for bicuculline to competitively antagonize the currents activated by halothane and GABA are similar (0.69 and 0.72 microM, respectively). These results indicate that halothane activates the alpha6 beta2 gamma2S GABA(A) receptor to induce a current similar to the GABA-induced current.

Animals↗

PubMed1996

The effects of halothane on arginine-vasopressin-induced Ca2+ mobilization from the intracellular stores and the receptor-mediated Ca2+ entry from the extracellular space in single cultured smooth muscle cells of rat aorta.

Halothane has a direct action on vascular smooth muscle cells and causes relaxation of these cells, yet neither the mechanism nor the site of its action is completely understood. Using digital imaging microscopy with the Ca2+ indicator fura-2, the effects of halothane on the intracellular [Ca2+] dynamics induced by arginine vasopressin (AVP) in the perinuclear region and cytosol in single cultured smooth muscle cells of rat aorta were studied. Changes in intracellular [Ca2+] were expressed as percent increases in the ratios of fluorescence intensity at 500 nm excited by 340 nm and 380 nm. AVP (10(-7) M) elicited an initial transient increase in [Ca2+] in the perinuclear region higher than that in the cytosol in Ca(2+)-containing solution (346% +/- 21% and 213% +/- 22%, respectively). Halothane, 0.5%, attenuated the [Ca2+] increase induced by AVP in the perinuclear region and cytosol, and halothane, 1.0% and 2.0%, abolished the differential increase. Under the continuous application of AVP (10(-7) M), Ca2+ restoration in the medium after perfusion with Ca(2+)-free solution increased the perinuclear [Ca2+] more than the cytosolic [Ca2+]. Both were significantly attenuated by 2.0% halothane, but not by nicardipine (10(-5) M) or ryanodine (10(-6) M). Our results suggest that halothane may attenuate the Ca2+ release from the intracellular Ca2+ stores more than the receptor-mediated Ca2+ entry from the extracellular space in the AVP-induced response in these cells.

Anesthetics, Inhalation↗

PubMed1997

Effects of epidural and intravenous buprenorphine on halothane minimum alveolar anesthetic concentration and hemodynamic responses.

There is limited information regarding the effects of epidural or intravenous (i.v.) buprenorphine on minimum alveolar anesthetic concentration (MAC) of volatile anesthetic and hemodynamic responses to tracheal intubation and surgical incision. This study was conducted to find the effects of i.v. and epidural buprenorphine required for postoperative pain relief on halothane MAC and hemodynamic responses to tracheal intubation and surgical incision in 126 female patients. Patients were randomly assigned to the four groups: Group I received i.v. and epidural saline as a control; Group II was given buprenorphine 4 micrograms/kg i.v.; and Groups III and IV received buprenorphine 2 and 4 micrograms/kg epidurally, respectively. Groups II-IV were divided into the two subgroups according to the timing of administration, either at induction of anesthesia in the operating room (OR) (OR group) or 90 min before anesthetic induction in the ward (Ward group). Anesthesia was induced with only halothane in oxygen, and the trachea was intubated without other drugs. Halothane MAC was determined by logistic regression analysis and the Dixon up-and-down method. Halothane MAC in the seven study groups was as follows: 0.75% +/- 0.05% (mean +/- SE) in Group I; 0.49% +/- 0.03% and 0.59% +/- 0.04%, respectively, in Groups II OR and Ward; 0.65% +/- 0.003% and 0.49% +/- 0.07%, respectively, in Groups III OR and Ward; and 0.51% +/- 0.07% and 0.37% +/- 0.02%, respectively, in Groups IV OR and Ward. Halothane MAC decreased significantly (P < 0.05) in groups that received buprenorphine except Group III-OR compared with Group I. Systolic blood pressure did not change significantly in Groups II-OR and IV-OR after tracheal intubation and in Group III-Ward and IV-Ward after surgical incision but increased significantly (P < 0.05) in the remaining groups in response to noxious stimuli. Heart rate responses to tracheal intubation and surgical incision were similar to those in systolic blood pressure. These results indicate that preanesthetic administration of epidural or IV buprenorphine required for postoperative analgesia reduces halothane MAC and attenuates hemodynamic responses to tracheal intubation and surgical incision according to the dose, route, and timing of administration.

Adult↗

PubMed1998

Halothane and isoflurane attenuate the relaxant response to nonadrenergic and noncholinergic nerve stimulation of isolated canine cerebral arteries.

UNLABELLED: Stimulation of nonadrenergic noncholinergic (NANC) nerves elicits relaxation of canine cerebral arteries via the nitric oxide (NO)-cGMP pathway. The purpose of this study was to investigate the effects of halothane and isoflurane on the relaxant response of isolated canine cerebral arteries to NANC nerve stimulation. The isometric tension of isolated canine cerebral arteries, which had been denuded of endothelium, was measured in a tissue bath. The application of transmural electrical stimulation (TES) at a frequency of 5 Hz elicited a transient relaxation of arteries partially contracted with prostaglandin F2alpha. This effect was abolished by treatment with N(G)-nitro-L-arginine (3 x 10[-5] M), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (10[-5] M), or tetrodotoxin (10[-6] M). Treatment with halothane (2.3%) or isoflurane (2.3% and 3.5%) attenuated the relaxant response to TES (P < 0.05). Halothane (2.3%) but not isoflurane (2.3% and 3.5%) attenuated relaxation induced by s-nitro-N-acetylpenicillamine. We suggest that halothane and isoflurane inhibit cerebroarterial vasodilation mediated via NO-cGMP pathway activated by stimulation of the NANC nerves. The sites of action of halothane and isoflurane on the NO-cGMP pathway may differ. IMPLICATIONS: Nonadrenergic noncholinergic nerves play a role in the regulation of vascular tone in cerebral arteries via the nitric oxide-cGMP pathway. This study showed that, in isolated canine cerebral arteries, halothane and isoflurane inhibit the relaxation caused by nonadrenergic noncholinergic nerve stimulation, but their sites of action may differ.

Animals↗

PubMed1999

Pretreatment with dexmedetomidine: altered indices of anesthetic depth for halothane in the neuraxis of cats.

UNLABELLED: The sedative and anesthetic-sparing ability of the alpha2-adrenergic agonist dexmedetomidine is well documented. In this study, we identified the effects of halothane, with and without dexmedetomidine, on hemodynamic and electroencephalographic (EEG) variables and quantified the concentration of halothane resulting in various anesthetic depth indices mediated through the central nervous system (CNS) in chronically instrumented cats. Halothane was given alone or after dexmedetomidine (15 microg/kg p.o.). In both groups, four indices of anesthetic depth--minimum alveolar anesthetic concentration (MAC; no movement to noxious stimuli), MAC(BAR) (no autonomic response to noxious stimuli), MAC(BS) (EEG burst suppression), and MAC(ISOELECTRIC) (EEG isoelectricity)--were determined. Halothane decreased arterial blood pressure, heart rate, and higher frequency components of the EEG before the onset of burst suppression and isoelectricity. Dexmedetomidine pretreatment augmented the actions of halothane on arterial pressure, heart rate, and the EEG. Dexmedetomidine reduced the halothane concentrations resulting in MAC (from 1.22% +/- 0.06% to 0.89% +/- 0.08%) and MAC(BAR) (from 1.81% +/- 0.05% to 1.1% +/- 0.10%), but not those resulting in MAC(BS) (3.01% +/- 0.17% vs 3.14% +/- 0.10%) or MAC(ISOELECTRIC) (4.39% +/- 0.26% vs 4.65% +/- 0.12%). These results suggest that dexmedetomidine does not alter various CNS-mediated indices of anesthetic action to equivalent degrees and that there are dissimilar degrees of an anesthetic-sparing action at different levels of the neuraxis. IMPLICATIONS: The anesthetic adjuvant dexmedetomidine seems to differentially alter central nervous system-mediated indices of anesthetic action. Lower brainstem or spinal determinants of anesthetic depth (movement and hemodynamic responses) are more attenuated than those of higher brain functions, such as the electroencephalogram.

Adrenergic alpha-Agonists↗

PubMed1999

Halothane stimulates a Na+H+ antiporter involved in the regulation of intracellular pH in alveolar epithelial cells.

UNLABELLED: Changes in intracellular pH (pHi) of alveolar type II (ATII) cells have been involved in the pathophysiology of pulmonary edema. ATII cells have evolved several ions transporters to regulate their pHi, including a Na+H+ antiporter. Because halothane alters the activity of ion transporters in various cells types, it may also affect the activity of this Na+H+ antiporter. This study was performed 1) to characterize a Na+H+ antiporter in a model of ATII cells and 2) to investigate the effect of halothane on the activity of this antiporter. ATII cells were obtained from primary rat ATII cells transfected with a mutant of simian virus SV40 large T antigen (SV40-T2), and their pHi was monitored using the pH-sensitive fluorescent probe 2'-7' (bis carboxyethyl)-5(6')-carboxyfluorescein. We demonstrated in vitro that 1) a Na+H+ antiporter (apparent Km 6.8 +/- 3.4 mM, Vmax 0.0105 +/- 0.0013 delta UpHi/s) regulates the pHi of SV40-T2 cells and 2) at clinically relevant concentrations (10(-3) to 10(-5) M) and for a short exposure duration (60 min), halothane enhances the activity of this antiporter. Because ATII cell acidification has been associated with alterations in the alveolar epithelial barrier, halothane-induced intracellular alkalinization might exhibit some protective effect in clinical situations, such as aspiration pneumonia. IMPLICATIONS: In vitro, halothane induces an intracellular alkalinization of pneumocytes II via the activation of a Na+H+ antiporter. Because acidification of these cells has been associated with alterations in the alveolar epithelial barrier, halothane might exhibit some protective effect in clinical situations, such as aspiration pneumonia.

Anesthetics, Inhalation↗

PubMed2001

The effects of sevoflurane and halothane anesthesia on cerebral blood flow velocity in children.

UNLABELLED: We compared cerebral blood flow velocity during anesthesia with sevoflurane and halothane in 23 children admitted for elective surgery (age, 0.4-9.7 yr; median age, 1.9 yr; ASA physical status I-II). Inhaled induction was performed in a randomized sequence with sevoflurane or halothane. Under steady-state conditions, cerebral blood flow velocity (systolic [V(s)], mean [V(mn)], and diastolic [VD]) were measured by a blinded investigator using transcranial pulsed Doppler ultrasonography. The anesthetic was then changed. CBFV measurements were repeated after washout of the first anesthetic and after steady-state of the second (equivalent minimal alveolar concentration to first anesthetic). The resistance index was calculated. VD and V(mn) were significantly lower during sevoflurane (V(mn) 1.35 m/s) than during halothane (V(mn) 1.50 m/s; P = 0.001), whereas V(s) was unchanged. The resistance index was lower during halothane (P < 0.001). Our results indicate lower vessel resistance and higher mean velocity during halothane than during sevoflurane. IMPLICATIONS: The mean cerebral blood flow velocity is significantly decreased in children during inhaled anesthesia with sevoflurane than during halothane. This might be relevant for the choice of anesthetic in children with risk of increased intracranial pressure, neurosurgery, or craniofacial osteotomies.

Anesthetics, Inhalation↗

PubMed2002

Halothane potentiation of hydrogen peroxide-induced inhibition of surfactant synthesis: the role of type II cell energy status.

UNLABELLED: Small concentrations of inhaled anesthetics can affect Type II cell surfactant production and exacerbate oxidant-mediated lung injury. We hypothesized that inhaled anesthetics augment oxidant-induced Type II pneumocyte dysfunction related to their different effects on cellular adenosine triphosphate (ATP) status. Freshly isolated Type II cells were exposed to different concentrations of hydrogen peroxide (H2O2) in the presence or absence of an in vitro halothane exposure. Cells exposed to 100 microM H2O2 alone demonstrated a 23% decrease in ATP levels and a 32% decrease in phosphatidylcholine (PC) synthesis compared with controls. Halothane alone decreased PC synthesis by only 12% and reduced ATP levels by 20%. However, when exposed to both halothane and H2O2 together, ATP levels decreased by 40%, and PC synthesis rates decreased by 51%. Pretreatment of cells with nicotinamide, an inhibitor of poly adenosine diphosphate ribose polymerase, completely prevented the ATP loss and PC synthesis decline caused by H2O2 alone, but it had no effect on the halothane-augmented portion of the cell injury. These data suggest that the ability of halothane to enhance oxidative damage may be related to its own specific effects on cell energetics that may not be amenable to the same treatments used to mitigate other cellular mechanisms of oxidative stress. IMPLICATIONS: A mediator of inflammation (hydrogen peroxide) and an inhaled anesthetic (halothane) interact to decrease cell energy and secretion of a substance (surfactant) required for healthy lung function from cells that line gas-exchange compartments. This interaction represents a possible mechanism by which inflammatory lung disease may become more severe intraoperatively.

Adenosine Triphosphate↗

PubMed2002

Duration of preoperative fast correlates with arterial blood pressure response to halothane in infants.

UNLABELLED: In this study, we sought to determine whether the duration of preoperative fasting affects the decrease in blood pressure observed in infants and children during halothane anesthesia. Two-hundred-fifty pediatric patients were divided into 5 age groups: term neonates (n = 50), 1-6 mo (n = 50), 6-24 mo (n = 50), 2-6 yr (n = 50), and 6-12 yr (n = 50). After anesthetic induction with halothane, end-tidal halothane was maintained at 2 minimum alveolar anesthetic concentration (MAC) for 10 min to allow myocardial uptake. Patients were grouped by duration of preoperative fast (0-4 h, 4-8 h, 8-12 h, and >12 h). Changes in heart rate and systolic (SAP) and mean (MAP) arterial blood pressure from preinduction to 2 MAC were compared among fasting groups within each age group. In the 1- to 6-mo age group, the changes in SAP and MAP were significantly greater in infants fasting 8-12 h than in those fasting 0-4 h (SAP, -51 mm Hg versus -31 mm Hg, respectively; MAP, -48 mm Hg versus -32 mm Hg; P < 0.05). No statistically significant differences were noted in the older age groups. The results of this study demonstrate that prolonged preoperative fasting is associated with a greater decrease in blood pressure in infants. This exacerbation of the already significant hemodynamic depression observed in infants during halothane anesthesia underscores the importance of adherence to published fasting guidelines. IMPLICATIONS: We studied changes in blood pressure during halothane anesthesia in infants and children and found that blood pressure decreased to a greater extent in infants who fasted for longer than 8 h before surgery. This exacerbation of the already significant hemodynamic depression observed in infants during halothane anesthesia underscores the importance of adherence to published fasting guidelines.

Anesthetics, Inhalation↗

PubMed1975

Urinary metabolites of halothane in man.

The urinary metabolites of halothane (2-bromo-2-chloro-1,1,1-trifluoroethane) were investigated in five individuals given trace doses (25 muCi), and in three individuals given large doses (1 mCi) of radioactively labeled 14C-halothane. The latter were donor subjects for heart transplant operations. Separation of the nonvolatile urinary metabolites of halothane was accomplished by chemical extraction, electrophoresis, ion-exchange and high-pressure liquid chromatography, and gas chromatography. Identification of the individual metabolites was by nuclear magnetic resonance and mass spectrometry. Three major metabolites were identified: trifluoroacetic acid, N-trifluoroacetyl-2-aminoethanol, and N-acetyl-S-(2-bromo-2-chloro-1,1-difluoroethyl)-L-cysteine. Smaller unidentified radioactive peaks were also found. The presence of both ethanolamide and cysteine conjugates of halothane is of concern. These urinary products imply the presence of reactive intermediates. The conjugation of such intermediates to proteins and phospholipids may give rise to the high-molecular-weight covalently bound metabolites demonstrated to be present in the liver following halothane anesthesia. Elucidation of the structures of the urinary metabolites provides information important to an understanding of halothane metabolism and its potential hepatotoxicity.

Binding Sites↗

PubMed1976

Halothane action on lymphocytes does not involve cyclic AMP.

Both theophylline and halothane inhibited transformation of human lymphocytes by phytohemagglutinin (PHA). Theophylline did not augment the inhibitory action of halothane and depressed PHA transformation of halothane-treated cells to the same extent as that of air-treated cells. Halothane- and air-treated lymphocytes, prior to PHA addition, had the same content of cyclic AMP. The addition of PHA to these cultures raised cyclic-AMP concentrations to the same extent in halothane- and air-treated lymphocytes. Halothane action on PHA-stimulated lymphocytes appears not to involve changes in cyclic nucleotide metabolism.

Cells, Cultured↗

PubMed1976

Halothane-induced decrease in experimental myocardial ischemia in the non-failing canine heart.

The effect of halothane on net myocardial oxygen balance of ischemic myocardium was studied in the non-failing canine heart. Myocardial ischemia was produced by repeated reversible occlusions of a coronary artery; the severity of ischemia was estimated by summating ST-segment elevations (sigma ST) obtained by epicardial ECG mapping at 15 to 18 sites. Control measurements were obtained before and after administration of halothane (0.75 per cent) to six dogs with chloralose-urethane basal anesthesia. Halothane was associated with significant decreases of systemic arterial pressure (P less than .001), heart rate (P less than .01), and the product of systolic arterial pressure X heart rate (P less than .01), an indirect index of myocardial oxygen consumption, while left atrial pressure remained unchanged at normal levels. sigmaST during occlusion was less (P less .001) during halothane (26.5 +/- 7.4 (SD) mv) than before (36.6 +/- 5.4 mv) or after (34.4 +/- 8.2 mv) its administration. Thus, halothane decreased the severity of experimentally-induced myocardial ischemia in the non-failing canine heart. The data suggest that, in the absence of ventricular failure, halothane influences the relationship between myocardial oxygen supply and demand in a favorable direction when coronary blood flow is limited.

Anesthesia, General↗

PubMed1977

Cultured neuroblastoma cells and halothane: effects on cell growth and macromolecular synthesis.

Cultured mouse neuroblastoma cells were grown in air-CO2 or air-CO2-halothane-gassed incubators. In the presence of halothane the growth rate of the cells was inhibited in a dose-dependent manner; 2 per cent halothane completely inhibited cell growth, while at 0.3 per cent halothane, the growth rate was 74 per cent of the control rate. The biosynthesis of protein and RNA in cells grown in the control atmosphere and that in cells grown in 1 per cent halothane were compared by several techniques. No significant difference between the rates of synthesis of these two macromolecules could be detected. Furthermore, a comparison of labeled protein and RNA by SDS-polyacrylamide gel electrophoresis revealed no qualitative difference. From this and previous work it is concluded that halothane affects the morphology and growth rate of cultured mouse neuroblastoma cells by disrupting cytoplasmic actin-like micro-filaments.

Animals↗

PubMed1977

Volatile metabolites of halothane in the rabbit.

To date, carbon dioxide is the only volatile metabolite that has been identified to result from the biotransformation of halothane. This study was undertaken to determine whether other volatile metabolites might be formed. Expiratory gas from four rabbits given halothane by inhalation and from three rabbits into which the halothane was injected intraperitoneally was analyzed by gas chromatography. Qualitative analysis of the metabolites was made by injecting 50-70 microliter of the expired halothane condensed in an ultralow-temperature device (-80 C) attached to the mass spectrometer. Gas chromatography revealed two volatile metabolites between the air peak and the halothane peak. They were identified by mass spectra to be CF2:CHCl and CF2CH2Cl. These volatile metabolites appeared immediately after the beginning of anesthesia. The present investigation suggests the possible existence of a previously unknown metabolic pathway of defluorination and debromination occurring in the early stage of halothane biotransformation. These volatile metabolites may be toxic, highly reactive intermediates that undergo further biotransformation.

Animals↗

PubMed1979

Halothane mimics oxygen in oxygen microelectrodes.

The effects of halothane and enflurane on the polarographic measurement of oxygen with five platinum and three gold microelectrodes were examined. Oxygen microelectrodes were calibrated in saline solution equilibrated with either nitrogen (N2) or air, then either halothane, 1.0 per cent, or enflurane, 2.0 per cent, was added to the gas mixture. For each electrode, polarographic curves were determined during exposure to five equilibrating gas mixtures: N2, air, N2 plus halothane, air plus halothane, and N2 plus enflurane. Halothane variably increased the current produced (and therefore the estimated oxygen tension) at all polarizing voltages in saline solution equilibrated with either N2 or air. The effect was present in both conical platinum electrodes and recessed-tip gold electrodes and was not prevented by membrane coatings of polystyrol, Rhoplex or collodion. Enflurane did not alter the polarographic measurement of oxygen. It is concluded that tissue oxygen tension measurements, made with these microelectrodes and membranes, may be unreliable in the presence of halothane.

Calibration↗

PubMed1979

Sites and mechanisms of action of halothane on skeletal muscle function in vitro.

In isolated rat diaphragm strips, halothane augments the tension produced during caffeine-induced contractures in a dose-related manner. Potassium-induced contracture tension is augmented in the presence of halothane to a concentration of 0.75 per cent, and decreased at halothane concentrations of more than 1 per cent. The time of peak tension for potassium-induced contractures is diminished by all halothane concentrations. T-tubular disruption by hypertonic glycerol does not alter anesthetic-induced augmentation of caffeine-induced contractures. It is postulated that halothane augments calcium-release processes in sarcoplasmic reticulum. Membrane events or excitation-contraction coupling steps may be also altered by halothane.

Animals↗

PubMed1980

Effects of halothane on glucose-stimulated insulin secretion and glucose oxidation in isolated rat pancreatic islets.

Previous studies have shown that halothane inhibits glucose-stimulated insulin secretion. This study was designed to determine whether the mechanism of inhibition involves a reduction in glucose metabolism. The effects of halothane on glucose (16.7 mM)-stimulated insulin secretion and glucose oxidation were studied in isolated rat pancreatic islets. Halothane, 0.11 mM (0.5 MAC), 0.22 mM (1.0 MAC), and 0.33 mM (1.5 MAC), inhibited glucose-stimulated insulin release in a dose-related manner by 5.2 per cent (NS), 21.0 per cent (P < 0.05), and 32.6 per cent (P < 0.01), respectively. At the 0.33 mM (1.5 MAC) concentration, halothane did not significantly inhibit the oxidation of 6-14C-glucose to 14CO2, although higher concentrations of halothane did result in significant inhibition. The data suggest that halothane's inhibitory effect on glucose-stimulated insulin secretion is not due to interference with glucose oxidation.

Anesthesia, Inhalation↗

PubMed1980

Effects of halothane on spinal neuronal responses to graded noxious heat stimulation in the cat.

This study was undertaken to examine the dose-response effects of clinical concentrations of halothane on activity of wide-dynamic-range (WDR) neurons in the dorsal horn of the spinal cord of the decerebrate, spinal cord-transected cat. All cells (n = 40) responded maximally to high-intensity (greater than 45 C) noxious heat stimulation. Following administration of halothane, 0.5, 1.0, and 1.5 per cent, the mean spontaneous discharge frequency was significantly decreased (P < 0.01) by 44, 74, and 87 per cent, respectively. The mean evoked discharge frequencies were also significantly decreased at all temperatures (46, 48.5 51 C) by all concentrations of halothane. The slope of the regression line relating heat intensity and evoked neuronal discharge frequency was significantly decreased (P < 0.01) with both 1.0 and 1.5 per cent halothane by 46 and 75 per cent, respectively. Since the spinal cord was transected, these results indicate that these effects were the result of a direct action at the level of the spinal cord. The neuronal activity that was suppressed was evoked by stimuli that were exclusively noxious. This substantiates the ability of halothane to modify the transmission of noxious information at the spinal cord level, and thus explains a mechanism by which halothane may induce analgesia.

Animals↗