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PubMed2003

The postoperative effects of halothane versus isoflurane on hepatic artery and portal vein blood flow in humans.

UNLABELLED: Animal studies have shown that halothane decreases total hepatic blood flow (THBF) by reducing both arterial (HABF) and portal (PVBF) inflow, whereas isoflurane appears to preserve them. In this study we assessed the effect of halothane and isoflurane on HABF and PVBF in surgical patients by using the pulsed Doppler technique. A validation study was conducted in six cynomolgus monkeys to compare the values of THBF obtained by the pulsed Doppler and indocyanine green clearance methods. Subsequently, six patients (ASA status I and II) undergoing elective open cholecystectomy were studied after surgery by using implanted pulsed Doppler probes. THBF and liver flow partition were compared during 1% halothane and 1.5% isoflurane (end-tidal concentrations). In the animal study, there was good agreement between the techniques (Bland and Altmann representation). In flunitrazepam-anesthetized patients, THBF was 1120 +/- 284 mL/min. Compared with this baseline and for a similar mean arterial blood pressure decrease (10%), THBF was maintained with isoflurane, whereas it decreased by 36% (P < 0.05) under halothane. With isoflurane, PVBF increased (25%; P = 0.067) with a maintained HABF. With halothane, both PVBF (-44%; P < 0.05) and HABF (-20%; P < 0.05) were reduced. Halothane acted mainly as a vasoconstrictor of the hepatic circulation, whereas isoflurane was a vasodilator, confirming the beneficial effect of isoflurane on hepatic oxygen supply. IMPLICATIONS: Volatile anesthetics may alter liver circulation with serious adverse effects. Using implanted pulsed Doppler probes in six anesthetized patients, we showed that halothane acted mainly as a vasoconstrictor of the liver vascular bed, whereas isoflurane was a vasodilator, confirming the beneficial effect of isoflurane on liver oxygen supply.

Adult↗
PubMed2004

The effects of halothane, isoflurane, and sevoflurane on Ca2+ current and transient outward K+ current in subendocardial and subepicardial myocytes from the rat left ventricle.

Halothane, isoflurane, and sevoflurane abbreviate ventricular action potential duration (APD), and for halothane this effect is greater in the subendocardium than in the subepicardium. In this study we investigated mechanisms underlying the regional effects of these anesthetics on APD. The effect of 0.6 mM halothane, isoflurane, and sevoflurane on the action potential, L-type Ca(2+) current, transient outward K(+) current (I(to)), and steady-state current was recorded in rat left ventricular subendocardial and subepicardial myocytes. Halothane and isoflurane (but not sevoflurane) reduced APD significantly (P < 0.05), more in subendocardial than subepicardial myocytes. Peak L-type Ca(2+) current did not differ between regions and, compared with control, was reduced significantly in both regions by 40% (P < 0.001), 20% (P < 0.001), and 12% (P < 0.01) by halothane, isoflurane, and sevoflurane, respectively. I(to) was greater in subepicardial (3.95 +/- 0.29 nA) than subendocardial (1.12 +/- 0.05 nA) myocytes. In subepicardial myocytes, peak I(to) was reduced significantly by halothane (P < 0.01) and isoflurane (P < 0.05) (by 8% and 7%, respectively) but was unaffected by sevoflurane. No significant reduction of I(to) was observed in subendocardial myocytes with the three anesthetics. The steady-state current was increased significantly (P < 0.05), but the extent of this increase did not differ between the two regions or among the three anesthetics. Therefore, greater inhibition of I(to) in subepicardial than subendocardial myocytes by halothane and isoflurane could underlie their transmural effects on APD.

Action Potentials↗
PubMed2006

The differential effects of halothane and isoflurane on electroencephalographic responses to electrical microstimulation of the reticular formation.

Isoflurane and halothane cause electroencephalographic (EEG) depression and neuronal depression in the reticular formation, a site critical to consciousness. We hypothesized that isoflurane, more than halothane, would depress EEG activation elicited by electrical microstimulation of the reticular formation. Rats were anesthetized with either halothane or isoflurane and stimulating electrodes were positioned in the reticular formation. In a crossover design, anesthetic concentration was adjusted to 0.8 and 1.2 minimum alveolar concentration (MAC) of halothane or isoflurane and electrical microstimulation was performed and the EEG responses were recorded. Microstimulation increased the spectral edge and median edge frequencies 2-2.5 Hz at 0.8 MAC for halothane and isoflurane and 1.2 MAC halothane. At 1.2 MAC isoflurane, burst suppression occurred and microstimulation decreased the period of isoelectricity (24% +/- 19% to 8% +/- 7%; P < 0.05), whereas the spectral edge and median edge frequencies were unchanged. At anesthetic concentrations required to produce immobility, the cortex remains responsive to electrical microstimulation of the reticular formation, although the EEG response is depressed in the transition from 0.8 to 1.2 MAC. These data indicate that cortical neurons remain responsive to synaptic input during isoflurane and halothane anesthesia.

Anesthetics, Inhalation↗
PubMed1984

Comparison of systemic and cerebrovascular effects of isoflurane and halothane.

This study was carried out to compare the cerebral and systemic circulatory effect of halothane and isoflurane. Six mongrel dogs were anesthetized with 1.3 minimal alveolar concentration (MAC) (1%) halothane and were compared with six mongrel dogs anesthetized with 1.3 MAC (1.5%) isoflurane. Likewise, 6 dogs anesthetized with 1.7 MAC (1.3%) halothane were compared with 6 dogs anesthetized with 1.7 MAC (2%) isoflurane. Blood flow (using the radioactive microsphere technique) and cardiovascular measurements were obtained 2 hours after the induction of anesthesia and were repeated 5 more times at hourly intervals. The heart rate was similar in all groups of dogs, except that it was significantly lower with 1.7 MAC halothane. The mean arterial pressure was statistically higher with isoflurane at both concentrations than with halothane. The cardiac index was similar in all groups, except with 1.7 MAC isoflurane, when it was higher. At the early measurements, total cerebral blood flow (CBF) was above "normal" levels in all groups. At 1.3 MAC, the total CBF tended to be lower with isoflurane, but did not reach statistically significant levels. Blood flow decreased over time in all groups. The cerebral vascular resistance (CVR) mirrored the changes in blood flow, showing no difference between agents at 1.7 MAC, but the CVR with isoflurane was significantly higher at 1.3 MAC than it was with halothane. Regional cerebral blood flow showed marked differences. Regional flow to the hemispheres and the cortical gray matter showed that isoflurane tended to produce lower blood flow, particularly at the 1.3 MAC concentration. The reverse was true in the posterior fossa structures, with the brain stem and cerebellum showing higher blood flows with isoflurane, particularly at 1.7 MAC. Isoflurane may have several advantages over halothane for neurosurgical procedures.

Animals↗
PubMed1998

Changes of hepatic tissue phospholipid peroxidation, malondialdehydes, and antioxidative enzyme activities in dogs with halothane inhalation.

To elucidate the pathogenesis of halothane-induced hepatopathy, the changes of hepatic tissue phospholipid peroxidation, malondialdehydes (MDAs), and antioxidative enzyme activities were examined in the portal vein arterialized dogs with halothane inhalation. In group A, which was given halothane inhalation under the hepatic blood flow volume less than 10% of pre-operation volume designated as a hypoxic condition, peroxidized phosphatidylcholine (PC), and free and protein-bound MDA levels significantly increased after inhalation. Although the level of protein bound MDA in group C, given hypoxic condition alone, also increased during the experimental period, the response of this was smaller than that in group A, suggesting that the halothane inhalation enhanced free radical generation under the hypoxic condition. In contrast, no significant changes of these levels were observed in groups B and D, both of which were supplied with sufficient hepatic oxygen as the normoxic condition. In addition, the significant negative correlations between hepatic oxygen supply and total or protein-bound MDA were observed in only halothane inhaled group. These findings suggested that the cause of halothane-induced hepatopathy is closely related to free radicals mainly generated from halothane anaerobic metabolism under the hypoxic condition.

Administration, Inhalation↗
PubMed2002

Effect of hypoxia on parathyroid hormone in lactating and neonatal rats: interaction with halothane.

Low oxygen in the blood (hypoxemia) may occur in the neonate or women in the postpartum period. Administration of inhalation anesthetic may be required in this period. The purpose of this study was to evaluate the effect of 7 d of hypoxia on the neonatal rat pup and lactating dam without or with acute halothane anesthesia on serum calcium and calciotropic hormones. Ionized calcium was not altered by hypoxia or halothane administration. Hypoxia from birth had no effect on serum parathyroid hormone (PTH) in 7-d-old rat pups (48+/-4 pg/mL). Halothane increased PTH in rat pups (74+/-8 pg/mL). The effect of halothane was not augmented in hypoxic pups. Hypoxia for 7 d had no effect on serum PTH in lactating dams (23+/-3 pg/mL). Halothane resulted in an increase in PTH (106+/-17 pg/mL). When halothane was administered to hypoxic lactating dams, a striking increase in serum PTH was observed (401+/-50 pg/mL). We hypothesize that halothane and hypoxia alter parathyroid gland function by a direct effect on cellular calcium dynamics. This interaction may have clinical significance in hypoxic patients requiring general anesthesia.

25-Hydroxyvitamin D 2↗
PubMed2000

The effect of the Halothane and Rendement Napole genes on carcass and meat quality characteristics of pigs.

The objective of this study was to determine the effects of the Halothane (N) and Rendement Napole (RN) genes on carcass and meat quality characteristics in pigs. Halothane and RN carrier (Nn/RN- rn+) Hampshire boars (n = 4) were mated to dams that were homozygous for the normal allele of both genes (NN/rn+ rn+) to produce progeny of four genotypes: 1, NN/rn+ rn+ (n = 31); 2, Nn/rn+ rn+ (n = 27); 3, NN/RN- rn+) (n = 30); and 4, Nn/RN- rn+ (n = 23). A DNA test was used to determine Halothane genotype, and longissimus glycolytic potential was used to predict the RN genotype. Pigs were reared under standard conditions to approximately 120 kg live weight and slaughtered at a commercial plant, and carcass characteristics and meat quality were evaluated. Halothane carriers (Nn/ _ _), in comparison to Halothane normal (NN/_ _) pigs, had shorter carcasses, lower longissimus ultimate pH, higher Minolta L* and b* values, and greater drip loss. Rendement Napole gene carriers (_ _/RN- rn+) had higher L* and b* values and drip and cooking loss and lower longissimus ultimate pH than homozygous recessive animals (_ _/rn+ rn+). There were Halothane x RN genotype interactions (P < 0.05) for subjective color, firmness, and marbling scores, and for shear force. Animals that were normal for both genes (NN/rn+ rn+) had the highest subjective scores for color (2.60, 1.88, 1.85, and 1.95, SE = 0.181, P < 0.05), firmness (2.53, 2.03, 2.10, and 1.89, SE = 0.182, P < 0 .05), and marbling (2.11, 1.44, 1.53, and 1.55, SE = 0.153, P < 0 .05) for genotypes 1, 2, 3, and 4, respectively, suggesting darker, firmer muscle with a higher level of marbling for this genotype. Shear force was highest for Nn/rn+ rn+ animals (3.83, 4.41, 3.79, and 3.70, respectively, SE = 0.172, P < 0.05). Gilts had less s.c. backfat thickness, greater longissimus muscle area, and lower subjective marbling scores than barrows. There was no effect (P > 0.05) of gender on other meat quality traits. This study illustrates the negative effects of the Halothane and RN genes on fresh pork quality and suggests that in combination the detrimental effects of the two genes are additive for ultimate pH, objective color, and water-holding capacity.

Alleles↗
PubMed1999

Comparison of recovery characteristics of sevoflurane and halothane for outpatient surgery in infants.

BACKGROUND: Sevoflurane, a newly approved potent inhaled anesthetic in Taiwan, provides rapid emergence from anesthesia in adults and children. Clinically, it is difficult to accurately assess the rate of recovery from anesthesia in infants. This study was designed to compare the emergence characteristics of halothane with those of sevoflurane having recourse to a respiratory agent monitor in infants undergoing outpatient surgery. METHODS: Forty infants of ASA class I, scheduled for day-case urologic surgery were studied. Patients were randomly allocated to two groups of 20. Sevoflurane or halothane was used as the inhaled anesthetic. Toward the end of surgery, sevoflurane or halothane was turned off. The concentrations of exhaled sevoflurane or halothane were read every minute after its discontinuation until extubation. The decay curve of the exhaled concentration of either agent was recorded minute by minute for 10 minutes. The time intervals from discontinuation of the inhalation agent to spontaneous movement and tracheal extubation were recorded. Untoward side-effects during emergence were also compared. RESULTS: Sevoflurane was eliminated faster than halothane. Based on the decay curves of the exhaled concentrations of the two agents, the time constant for halothane was 2.59 minutes and that for sevoflurane was only 1.43 minutes. The time from discontinuation of agent to extubation was also shorter for sevoflurane. Postoperative restlessness or agitation occurred more frequently in infants who received sevoflurane, although the difference was of no statistical significance. CONCLUSIONS: Sevoflurane is superior to halothane for rapid elimination in infant outpatient surgery as gauged by observation of end-tidal concentration elimination curves recorded with a respiratory agent monitor. No other postoperative side-effect was evident in sevoflurane anesthesia.

Ambulatory Surgical Procedures↗
PubMed1998

A prospective, randomized clinical comparison of sevoflurane and halothane in children.

BACKGROUND: The goal of the present multicenter investigation was to compare in a prospective and randomized study the induction, the maintenance and the recovery characteristics of halothane and sevoflurane when used in paediatric patients. METHODS: With the approval of the Ethical Committee and the parental written informed consent, 64 children aged 3-12 years, receiving general anaesthesia for urological, abdominal, and orthopaedic surgery, were studied. After oral flunitrazepam (0.05 mg kg-1), general anaesthesia was randomly induced by either sevoflurane (start: 1%, maximum: 7%, n = 32) or halothane (start: 0.5%, maximum: 4.5%, n = 32) and a 60% N2O in oxygen mixture until the loss of eyelash reflex (induction time). Then the trachea was intubated (if necessary, a muscle relaxant was administrated), and the concentrations of the anaesthetic vapours were adjusted in order to maintain cardiovascular stability until the end of surgery. The following times were recorded: time of extubation, time for having purposeful movements, time of eyes opening and readiness for discharge from the recovery area, as well as the occurrence of untoward events during either induction of, maintenance of, or recovery from anaesthesia. Before surgery and 24 hr after the procedure, blood was collected in order to measure serum creatinine and BUN. RESULTS: No differences in induction time, extubation time, side effects and postoperative renal function were observed between the two groups. Four patients in each group received muscle relaxants to perform intubation (p = NS). When compared to halothane group, children receiving sevoflurane had shorter times of showing purposeful movements (median: 9 min versus 15.5 min, p < 0.005), emergence from anaesthesia (median: 12 min versus 18 min, p < 0.05) and achieving readiness to be discharged (median: 18 min. versus 30 min, p < 0.005). Sevoflurane group also showed a more stable heart rate during the induction period than halothane one (p = 0.05). DISCUSSION: Sevoflurane is as effective as halothane in providing smooth and rapid induction of anaesthesia, while recovery is considerably faster and haemodynamic tolerance is better if compared to halothane; this suggests that sevoflurane could be an useful substitute for halothane in pediatric patients.

Adolescent↗
PubMed2001

Protective effect of halothane anesthesia on retinal light damage: inhibition of metabolic rhodopsin regeneration.

PURPOSE: To determine whether the volatile anesthetic halothane protects against light-induced photoreceptor degeneration in the rodent retina. METHODS: Albino mice and rats were anesthetized with halothane and exposed to high levels of white or blue light. Nonanesthetized animals served as controls. Retinal morphology was assessed by light microscopy, and apoptosis of photoreceptor cells was verified by detection of fragmented genomic DNA and in situ staining of apoptotic nuclei (TUNEL assay). Rhodopsin regeneration after bleaching was determined by measuring rhodopsin levels in retinas of mice or rats at different time points in darkness. RESULTS: Halothane anesthesia reversibly inhibited metabolic rhodopsin regeneration and thus prevented rhodopsin from absorbing high numbers of photons during light exposure. Consequently, photoreceptors of mice and rats anesthetized with halothane were completely protected against degeneration induced by white light. In remarkable contrast, however, halothane anesthesia did not protect against blue-light-induced photoreceptor cell death. CONCLUSIONS: After the initial bleach, halothane impeded photon absorption by rhodopsin by inhibiting metabolic rhodopsin regeneration. Apparently, the rhodopsin-mediated uptake of the critical number of photons to initiate white light-induced retinal degeneration was prevented. In contrast, halothane did not protect the retina against blue light. Blue light can efficiently restore functional rhodopsin from bleaching intermediates through a process termed photoreversal of bleaching. This process does not depend on the visual cycle via the pigment epithelium but nevertheless enables rhodopsin molecules to absorb the critical number of photons required to induce retinal degeneration.

Anesthesia, Inhalation↗
PubMed1976

Effects of halothane anesthesia on the biodisposition of ketamine in rats.

Ketamine, a highly lipophilic drug, was rapidly distributed into highly vascular organs and subsequently redistributed to less well perfused tissues, with concurrent hepatic metabolism and urinary and biliary excretion, after both i. m. and i. v. administration in the rat. Halothane, a potent cardiovascular depressant, was found to prolong the plasma and brain half-life of ketamine (50 mg/kg i.m.) and also increased the duration of ketamine-induced ataxia when the two drugs were administered concomitantly. Halothane anesthesia (0.8% halothane in oxygen) produced a decrease in the rate of uptake and delayed distribution and redistribution of ketamine (50 mg/kg i. m.), while the rate of urinary excretion of ketamine was not significantly altered. Similarly, redistribution of intravenously administered ketamine (30 mg/kg i. v.) was slowed in the presence of halothane. In vitro hepatic microsomal metabolism of ketamine and its principle N-demethylated metabolite, metabolite I, was inhibited noncompetitively by halothane with inhibitor constants (Ki) for halothane estimated to be 1.56 and 1. 64 mM,respectively. The gas anesthetic also decreased the overall rate of in vivo metabolism of ketamine (30 mg/kg i. v.) in a concentration-dependent manner. Thus halothane anesthesia by decreasing uptake, distribution, redistribution and metabolism of intramuscularly administered ketamine produced significant prolongation of its pharmacologic action on the central nervous system. Our results imply that concomitant use of inhalational anesthetics may prolong pharmacologic actions of other agents via effects on distribution/redistribution processes as well as on metabolism.

Anesthesia↗
PubMed2004

Cardiovascular changes during halothane induction in children.

OBJECTIVES: The incidence of bradycardia and myocardial depression following halothane induction in children is well documented. Bradycardia leads to reduced cardiac output, which can result in compromised organ perfusion. Halothane may sometimes induce arrhythmia. There is at present no study in this sub-region on the cardiovascular changes of halothane induction in children. This study was designed to investigate the cardiovascular changes and incidence of arrhythmias following halothane induction. PATIENTS AND METHODS: Ninety ASA I - II children aged 6 months to 12 years were studied. Premedication with oral promethazine 1mg/kg was given to all patients above the age of one year. Anaesthesia was achieved with incremental halothane up to 3% in 33% oxygen and nitrous oxide. Halothane induction led to a significant drop in SBP, DBP and MAP in all patients at the end of induction. (p < 0.005). Heart rate values were significantly less postinduction in children older than one year (p < 0.05). Arrhythmias occurred in 3.3% of all patients. No patient experienced bradycardia. Other complications included hypotension (8.8% ) and mild laryngeal spasm (2.2% ). RESULTS: Halothane induction in children results in significant reduction in heart rate and blood pressure. Bradyarrhthmias are uncommon with promethazine premedication.

Anesthesia, Inhalation↗
PubMed2006

[The effect of halothane or sevoflurane anesthesia on the extracellular concentration of dopamine and its metabolites examined by in vivo microdialysis techniques].

BACKGROUND: Volatile anesthetics induce changes in the extracellular concentration of dopamine (DA) metabolites in the rat striatum and their metabolism might be modified in different manners by different anesthetics. Although, we have studied DA metabolism during anesthesia using in vivo microdialysis techniques, time dimensional changes were not assessed concerning the difference between anesthetics. In the current investigation, the rats were anesthetized with halothane or sevoflurane, which has different blood solubility, and investigated the effect of anesthetics and time-related development on DA metabolism. METHODS: The rats were implanted with a microdialysis probe in the striatum and perfusate was introduced to HPLC every 20 min. Anesthesia was induced with halothane or sevoflurane for 20 or 60 min, and methamphetamine 2 mg x kg(-1) was administered during or after inhalation. RESULTS: Both anesthetic agents increased the concentration of DA metabolites, and dose and time dependency was more obvious with sevoflurane than with halothane. The increase of metabolites was prolonged after halothane anesthesia (20 min), but the effect of methamphetamine administered immediately after anesthesia on DA release was not enhanced by halothane anesthesia. Sevoflurane, not halothane anesthesia, antagonized methamphetamine-induced decrease of metabolites. CONCLUSIONS: Not only the difference of blood solubility between halothane and sevoflurane and anesthetic effect of time dependency, but also another pharmacological property affects DA metabolism, including the change in the activity of dopamine transporter during inhalation of anesthetics.

Anesthetics, Inhalation↗
PubMed1991

Immunomodulating effects of halothane in mice.

Twenty mice were acutely exposed to 1.5% halothane anaesthesia for 4 h. The mice were sequentially killed during the first 3 days after halothane exposure. Another 14 mice were chronically exposed to 0.25% halothane for 1 h daily, four times weekly for 3 months. The mice were sequentially killed every week. Acute exposure to halothane anaesthesia resulted in an increase in lymphocyte count per spleen, a decrease in serum IgG concentrations (Day 2), a reduction in spontaneous 3H-thymidine lymphocytic uptake (Day 1), and an increase in concanavalin-A-stimulated uptake. All immunometric assays returned to control levels on Day 3 after halothane exposure. Chronic non-anaesthetic concentrations of halothane exposure produced a decrease in serum IgG concentrations and an increase in spontaneous and stimulated lymphocyte 3H-thymidine uptake. It is concluded that acute exposure of mice to anaesthetic halothane results in a transient depression of the immune response, while chronic non-anaesthetic concentrations produce a differential effect on the two moieties of the immune system, a depressed humoral response and overactive cellular response.

Adjuvants, Immunologic↗
PubMed1991

Effects of halothane on impulse propagation in Purkinje fibers and at Purkinje-muscle junctions: relationship of Vmax to conduction velocity.

Alterations in Purkinje-to-muscle conduction may play a role in the development of cardiac arrhythmias. We compared the effects of halothane on impulse propagation in Purkinje fibers with its effects on impulse propagation across the Purkinje-muscle (P-M) junction. In canine Purkinje fibers, halothane (3%) significantly depressed conduction (P less than 0.05). Exposure to halothane altered conduction velocity (theta) in a manner predicted by cable theory; a significant correlation was noted between depression of Vmax and depression of the square of conduction velocity (theta 2) in Purkinje fibers exposed to 3% halothane (n = 11, r = 0.78, P less than 0.01). Halothane (3%) significantly slowed impulse propagation across the P-M junction (P less than 0.05). Vmax and the square of apparent P-M conduction velocity were not significantly correlated (n = 7, r = 0.34, P = 0.45). The data demonstrate that alteration of active membrane properties can account for halothane's slowing of conduction in Purkinje fibers but not for its slowing of conduction across the P-M junction. The data also suggest that a reduction in cell-to-cell coupling may contribute to depression of Purkinje-to-muscle conduction by halothane.

Action Potentials↗
PubMed1990

Effects of in vivo pretreatment with various barbiturates on anaerobic halothane metabolism in rat liver microsomes.

The effects of in vivo pretreatment with phenobarbital (PB), thiopental (TP), thiamylal (TA), pentobarbital (PT), and secobarbital (SB) on hepatic microsomal enzymes, and the effects on anaerobic halothane dehalogenation, aminopyrine N-demethylation, and aniline hydroxylation in the microsomes were studied in male Wistar rats. Three hundred twenty mumol/kg (0.1 ml) of PB, TP, TA, PT, SB, or 0.1ml of 0.9% saline were administered daily, intramuscularly, for periods of one day up to ten days. Daily administration of PB, TP, TA, or PT induced cytochrome P-450, NADPH-cytochrome P-450 reductase and/or cytochrome b5. However, administration of SB did not induce these enzymes. The potency of these enzyme inductions ranged in descending order as follows: PB, TP, TA, and PT. After five days of daily administration of PB, TP, or TA, the production of the anaerobic halothane metabolite, CDFE, increased to 187%, 134%, and 130% of the control, respectively. The production of another halothane metabolite, CTFE, likewise increased to 197%, 168%, and 163%. However, pretreatment with PT or SB had no effect on anaerobic halothane dehalogenation. Aminopyrine N-demethylation also increased after five days of daily administration of PB, TP, and TA. However, aniline hydroxylation decreased after five days of daily administration of TA. Other barbiturates had no effect on aniline hydroxylation. In this study we showed that whereas PT and SB did not enhance anaerobic halothane dehalogenation, PB, TP and TA did. We conclude that not only PB, and also TP and TA, may be enhancing factors in halothane hepatotoxicity. We recommend that, if barbiturates are necessary, SB and PT be used in the preadministration of halothane anesthesia.

Anaerobiosis↗
PubMed1990

Halothane increases cytosolic Ca2+ and inhibits Na+/H+ exchange in L6 muscle cells.

The effects of the general anesthetic halothane on the concentration of cytosolic free calcium ([Ca2+]i) and cytosolic pH (pHi), were investigated in L6 rat skeletal muscle cells. Basal [Ca2+]i was 169 +/- 8 nM, measured with the fluorescent Ca2(+)-indicator 1-[2-amino-5-(6-carboxyindol-2-yl)phenoxy]-2-(2'-amino-5- methylphenoxy)ethane-N,N,N',N'-tetra-acetate. Halothane (5.7 mM) increased [Ca2+]i to 225 +/- 15 nM in the presence of extracellular Ca2+, and from 137 +/- 6 nM to 179 +/- 9 nM in Ca2+ absence. This increase was dose-dependent. The anesthetic released about 50% of the releasable Ca2+ from intracellular stores. The resting pHi of L6 cells was 7.24 +/- 0.04, measured with the fluorescent pH indicator bis-carboxyethylcarboxyfluorescein. Halothane did not affect resting pHi, but inhibited cytoplasmic alkalinization by hypertonicity or cytoplasmic acidification: (1) The hypertonicity-induced alkalinization via activation of Na+/H+ exchange (to 7.50 +/- 0.08, initial rate 0.10 +/- 0.02 pH U/min) was inhibited with 5.7 mM halothane by 67%. (2) Acid-loaded cells (pHi 6.43 +/- 0.01 in cells) recovered towards neutrality via activation of Na+/H+ exchange (rate 0.47 pH U/min), and halothane inhibited the rate of pHi recovery by 50%. The halothane-mediated inhibition of alkalinizations after hypertonic exposure or acid-loading was also observed in bis-(o-amino-phenoxy)ethane-N,N,N',N'-tetra-acetate-loaded cells in Ca2(+)-free medium. Therefore, halothane increases [Ca2+]i and in parallel inhibits Na+/H+ exchange, compromising the ability of muscle cells to recover from imposed acidification.

Animals↗
PubMed1990

Ventricular arrhythmogenic dose of epinephrine in dogs and cats anesthetized with tiletamine/zolazepam and halothane.

The ventricular arrhythmogenic dose of epinephrine (ADE) was determined in 6 dogs anesthetized with halothane alone or with halothane after injection of tiletamine/zolazepam (TZ). Respiratory rate and tidal volume were controlled and sodium bicarbonate was administered to maintain arterial pH and blood gas values within reference range. Heart rate and arterial blood pressure were recorded during determination of the ADE. The ADE (mean +/- SD) was no different during anesthesia with use of halothane alone (8.9 +/- 4.3) than it was when injections of TZ preceded administration of halothane (6.7 +/- 2.8). Tiletamine/zolazepam was also administered IV immediately after determination of the ADE during halothane-induced anesthesia. The TZ administered in this manner did not alter the ADE. Blood pressure and heart rate were significantly greater during infusion of epinephrine than immediately prior to infusion. The administration of TZ did not alter blood pressure response. The ADE was also determined in 6 cats anesthetized with halothane preceded by administration of TZ. The ADE (mean +/- SD) was 0.7 +/- 0.23 micrograms/kg, a value similar to that reported for cats during anesthesia with halothane alone.

Anesthesia, Inhalation↗