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PubMed1988

Anaesthetic uptake and elimination: is there a difference between halothane and isoflurane in the dog?

In two groups of dogs, the uptake and elimination of halothane and isoflurane were studied using a closed-loop anaesthetic system which automatically controlled end-tidal halothane and isoflurane partial pressures at equi-MAC concentrations. Haemodynamic and respiratory variables were recorded and the anaesthetic partial pressures were measured in the inspired and expired air, as well as in the arterial, cerebrovenous and mixed venous blood. The controller delivered a higher inspired partial pressure of halothane than of isoflurane to compensate for the higher blood/gas partition coefficient. The partial pressures of halothane in the arterial, cerebrovenous and mixed venous blood increased at rates similar to those of isoflurane. During 160 min of uptake, the cerebral venous partial pressures remained significantly lower than the arterial partial pressures for both agents. On discontinuation of the anaesthetic, the partial pressures of halothane and isoflurane decreased at equal rates in arterial, cerebrovenous and mixed venous blood, and in end-tidal gas. It was concluded that the rate of uptake of isoflurane is more rapid than that of halothane from the alveolar space to the blood, but not from the blood to brain tissue. The rates of elimination from brain tissue and from blood were found to be similar for both agents.

Anesthesia, Inhalation↗

PubMed1988

Premedication with piroxicam in patients having dental surgery under general anaesthesia with halothane or isoflurane.

Pain, analgesic requirements, mouth opening and emesis were assessed in 60 patients who received either piroxicam 40 mg or placebo before dental surgery under general anaesthesia which included breathing either halothane or isoflurane. Patients went home on the day after surgery and completed a questionnaire concerning pain and emesis. There were four groups of 15 subjects: piroxicam-halothane, piroxicam-isoflurane, placebo-halothane or placebo-isoflurane. Pain increased at 2 and 4 h and had reduced by 18 h after surgery; there were no significant differences between the groups in pain scores. After operation, fewer patients in the piroxicam-isoflurane group required papaveretum compared with the piroxicam-halothane and placebo-halothane groups. Mouth opening was reduced between 2 and 4 h after surgery, but was less restricted after piroxicam-isoflurane than placebo-halothane. There was no difference between the groups in the incidence of emesis within 18 h of surgery. The postal questionnaire suggested that pain and emesis were reduced significantly during the 3 days after surgery in patients who had received piroxicam before surgery, compared with those who had received placebo.

Adult↗

PubMed1990

Halothane hepatitis: a case report.

This report describes a patient who required 12 anaesthetics over a period of 25 yr. Halothane was used on at least five occasions. The first documented halothane anaesthetic was followed by jaundice. Subsequently, he received at least four halothane anaesthetics, all of which were followed by illness attributable possibly to hepatotoxicity. He also received five nonhalothane anaesthetics, none of which was followed by postoperative illness. This case history shows strong evidence of halothane causing hepatotoxicity. It also shows an inverse relationship between the severity of the disease and the interval between halothane exposures. It is presented as evidence in favour of the advice on using halothane issued by the Committee on Safety of Medicines.

Anesthesia, Inhalation↗

PubMed1990

A urinary cysteine-halothane metabolite: validation and measurement in children.

An attempt was made in children to identify a urinary halothane-cysteine conjugate which had been described previously in adult patients following administration of halothane. If this conjugate was found it would indicate that a reductive metabolite of halothane binds covalently with the sulphydryl-containing amino acid, cysteine, a reaction which could lead to hepatic injury. The potential halothane-cysteine conjugate, N-acetyl-S-(2-bromo-2-chloro-1,1-difluoroethyl)-L-cysteine (acetyl BCFEC), was prepared and the identity of the compound established using hydrogen-1 and carbon-13 NMR spectroscopy and methane chemical ionization mass spectrometry. A measurement technique for acetyl BCFEC was developed using HPLC with u.v. detection at 200 nm. In six children after halothane anaesthesia, one child being studied twice, urine was collected for up to 1 week and analysed for acetyl BCFEC. Little or no acetyl BCFEC was detected in any of the 43 urine samples tested, indicating that in children it is not a significant urinary metabolite of halothane.

Acetylcysteine↗

PubMed1992

Effects of halothane and other volatile anaesthetics on protein synthesis and secretion in guinea pig liver slices.

We have investigated the effect of volatile anaesthetics on protein synthesis and secretion in Hartley male guinea pig liver slices. The slices (250-300 microns thick) were incubated in sealed roller vials containing Krebs-Henseleit buffer at 37 degrees C under 95% oxygen. Volatile anaesthetics were vaporized in the vials to produce constant concentrations in the medium. Halothane 1-2.1 mmol litre-1 produced a concentration-related decrease in protein synthesis (3H-leucine incorporation) and secretion. Deuterated halothane (d-halothane), which is less biotransformed, was less inhibiting than halothane: uptake of the 3H-leucine was not affected but its incorporation into the nascent peptide was inhibited. Enflurane 2.2 mmol litre-1, isoflurane 2.2 mmol litre-1 and sevoflurane 2.1 mmol litre-1 also inhibited protein synthesis, but to a lesser extent than halothane and d-halothane. We conclude that alterations in protein synthesis and secretion are an early and sensitive indicator of cellular injury by volatile anaesthetics in liver slices.

Anesthetics↗

PubMed1992

Halothane does not depress contractile function of fresh or fatigued diaphragm in pentobarbitone-anaesthetized dogs.

We have studied the effect of halothane on diaphragmatic contractile function by measuring transdiaphragmatic pressure (Pdi) and electromyogram of the diaphragm (Edi) during various stimulation frequencies in 15 pentobarbitone-anaesthetized dogs undergoing mechanical ventilation. We have examined also the effect of halothane on the fatigued diaphragm by repeating the measurements 5, 10, 15, 30, 60 and 90 min after 30 min of tetanic stimulation applied to the phrenic nerves. Administration of 1-2 MAC of halothane did not affect Pdi at any given stimulation frequency. Changes in the depth of halothane anaesthesia (0, 1 and 2 MAC) did not alter the force-frequency relationship of the diaphragm during recovery from fatigue. Edi was unaffected by halothane, except for a small decline during 100-Hz stimulation with 2 MAC. In contrast with the changes in Pdi, Edi during recovery from fatigue was the same as that determined before fatigue. It is concluded that halothane, in clinical concentrations, did not depress the contractile function of fresh or fatigued diaphragm in vivo.

Anesthesia, Intravenous↗

PubMed1994

Comparison of the effects of sevoflurane and halothane on the quality of anaesthesia and serum glutathione transferase alpha and fluoride in paediatric patients.

We have compared sevoflurane and halothane anaesthesia in paediatric patients with reference to induction and recovery. We also assessed hepatocellular integrity by measurement of serum glutathione transferase alpha (GSTA) concentration and sevoflurane metabolism by serum fluoride concentration. Fifty unpremedicated 5-12-yr-old children were allocated randomly to induction of anaesthesia via a face mask with 66% nitrous oxide in oxygen and sevoflurane (up to 7%) or halothane (up to 3.5%). Anaesthesia was maintained for 1.8 h at 1-1.2 MAC of the volatile agent. Children receiving sevoflurane had significantly faster induction and recovery variables than those receiving halothane. There was a small postanaesthetic increase in GSTA in both groups, suggesting that halothane and sevoflurane may disturb hepatocellular integrity. Serum concentrations of fluoride were significantly greater after sevoflurane than after halothane anaesthesia. There were no clinical signs or symptoms of hepatic or renal disturbance. Children tolerated sevoflurane better than halothane, which may have been because of the nonpungency of sevoflurane and the rapid psychomotor recovery after anaesthesia.

Anesthesia Recovery Period↗

PubMed1995

Comparison of the effects of sub-hypnotic concentrations of propofol and halothane on the acute ventilatory response to hypoxia.

To compare the effects of sub-anaesthetic concentrations of propofol and halothane on the respiratory control system, we have studied the acute ventilatory response to isocapnic hypoxia (AHVR) in 12 adults with and without three different concentrations of propofol and halothane. Target doses for propofol were 0, 0.05, 0.1 and 0.2 of the effective plasma concentration (EC50 = 8.1 micrograms ml-1). Target doses for halothane were 0, 0.05, 0.1 and 0.2 minimum alveolar concentration (MAC = 0.77%). The doses achieved experimentally were 0.01, 0.06, 0.13 and 0.26 of the EC50 for propofol and 0, 0.05, 0.11 and 0.20 MAC for halothane. During the experiment subjects breathed via a mouthpiece from an end-tidal forcing system. End-tidal PO2 (PE'O2) was held at 13.3 kPa for 5 min, and then at 6.7 kPa for 5 min. End-tidal PCO2 (PE'CO2) was held constant at 0.13-0.27 kPa greater than the subject's natural level throughout. The mean values for AHVR with propofol were: 12.8 (SEM 2.4) litre min-1 (0.01 EC50), 10.0 (1.9) litre min-1 (0.06 EC50), 9.8 (2.3) litre min-1 (0.13 EC50) and 4.9 (1.2) litre min-1 (0.26 EC50). The values for AHVR with halothane were: 11.9 (2.4) litre min-1 (0 MAC), 7.8 (1.6) litre min-1 (0.05 MAC), 5.9 (1.2) litre min-1 (0.11 MAC) and 3.2 (1.6) litre min-1 (0.2 MAC). The decline in AHVR with increasing dose for both drugs was statistically significant (ANOVA, P < 0.001); there was no significant difference between the two drugs with respect to this decline. Normoxic ventilation with propofol declined from 13.2 (1.6) litre min-1 (0.01 EC50) to 8.3 (0.9 litre min-1 (0.26 EC50), and with halothane declined from 13.5 (2.0) litre min-1 (0 MAC) to 11.8 (1.6) litre min-1 (0.2 MAC). This was significant for both drugs (ANOVA, P < 0.001).

Adolescent↗

PubMed1996

Sevoflurane-nitrous oxide or halothane-nitrous oxide for paediatric bronchoscopy and gastroscopy.

We have studied 120 infants and children, in three age groups (3-11 months, 1-5 yr and 6-15 yr), to compare anaesthesia with sevoflurane or halothane for bronchoscopy or gastroscopy, or both. Premedication or i.v. anaesthetic agents were not used. Patients were allocated randomly to receive either 7% sevoflurane or 3% halothane in 66% nitrous oxide in oxygen for induction of anaesthesia. The same inspired mixture was continued during bronchoscopy while the concentration of the inhalation agent was reduced by 50% during gastroscopy. Induction times were shorter for infants than for children and shorter for sevoflurane than for halothane. Cardiac arrhythmias were significantly more frequent during halothane than during sevoflurane anaesthesia. Physiological and psychomotor recovery were more rapid after sevoflurane than after halothane. At 24-h follow-up, children who received sevoflurane had significantly less nausea and vomiting. We conclude that sevoflurane was superior to halothane for paediatric bronchoscopy and gastroscopy.

Adolescent↗

PubMed1996

Hepatocellular integrity during and after isoflurane and halothane anaesthesia in surgical patients.

Subclinical disturbance in hepatocellular integrity, indicated by glutathione transferase Alpha (GSTA), has been associated with halothane, sevoflurane and propofol, but not with isoflurane anaesthesia. We anaesthetized 82 patients with isoflurane or halothane at 1 MAC for superficial surgery. GSTA concentration were measured with a sensitive time-resolved immunofluorometric assay in serum samples. GSTA concentrations increased from a baseline value of geometric mean 1.8 micrograms litre-1 (95% confidence intervals 1.4-2.2 micrograms litre-1) to a peak of 4.3 (3.3-5.7) micrograms litre-1 in the isoflurane group and from 2.1 (1.6-2.9) micrograms litre-1 to 6.2 (4.1-9.5) micrograms litre-1 in the halothane group. The change in GSTA was significant within groups but the difference between groups was not significant. Two patients exhibited an unexpectedly large increase in GSTA (peaks 370 and 620 micrograms litre-1) and a mild increase in alanine aminotransferase after halothane anaesthesia. We conclude that hepatocellular integrity was mildly disturbed after isoflurane and halothane anaesthesia but there was no difference between anaesthetics. Halothane anaesthesia may be associated with more advanced hepatocellular disturbance in some cases.

Adult↗

PubMed1998

Induction and emergence in infants less than 60 weeks post-conceptual age: comparison of thiopental, halothane, sevoflurane and desflurane.

We have studied 40 infants with a post-conceptual age of less than 60 weeks undergoing general anaesthesia for herniotomy. Patients were anaesthetized with 1 MAC equivalent values for age and agent and allocated randomly to receive halothane, savoflurane or thiopental for induction, and halothane, sevoflurane or desflurane for maintenance of anaesthesia. At induction, both time to acceptance of a face mask and loss of eyelash reflex were recorded. Emergence times were noted by a blinded observer. Induction and emergence times were similar between the halothane and sevoflurane groups but were consistently shorter in the desflurane group compared with the halothane or sevoflurane groups. There were no problems at extubation or significant apnoea in any group. Induction of anaesthesia in this population was no quicker with sevoflurane than with halothane and the method used for induction did not influence recovery time. Maintenance of anaesthesia with desflurane resulted in a shorter recovery time in infants in whom anaesthesia was induced with halothane or thiopental. Desflurane maintenance may be particularly beneficial in the neonate.

Anesthesia Recovery Period↗

PubMed1999

Mechanisms underlying the inotropic action of halothane on intact rat ventricular myocytes.

The mechanisms contributing to the negative inotropic effect of halothane were studied in isolated rate ventricular myocytes. Contraction and intracellular Ca2+ transients were measured optically in these cells. The initial application of halothane (2% or 0.5 mmol litre-1) led to short-lived increases in the Ca2+ transient and contraction, which were abolished by ryanodine. Continued application of halothane led to a sustained decrease in contraction: this resulted from: (i) a decrease in myofilament Ca2+ sensitivity; (ii) a decrease in the Ca2+ transient; and (iii) a decrease in the Ca2+ content of the sarcoplasmic reticulum. Although halothane reduced action potential duration, the sustained negative inotropic effect was similar when action potentials or voltage clamp pulses of constant duration were used to trigger contractions. In cells exposed to nifedipine 0.5 mumol litre-1 (which decreases the L-type Ca2+ current, ICa), Ca2+ transients, sarcoplasmic reticulum Ca2+ content and fractional release (the fraction of sarcoplasmic reticulum Ca2+ content released during each stimulus) were reduced. Halothane 0.5 mmol litre-1 (which also decreases ICa) decreased Ca2+ transients to a lesser extent and reduced sarcoplasmic reticulum Ca2+ content to a greater extent than nifedipine, whereas fractional release was unchanged compared with control. These data suggest that halothane sensitizes Ca(2+)-induced Ca2+ release from the sarcoplasmic reticulum in addition to reducing ICa.

Actin Cytoskeleton↗

PubMed1999

Concentration-dependent inotropic effects of halothane, isoflurane and sevoflurane on rat ventricular myocytes.

We have described the concentration-dependent inotropic effects of halothane, isoflurane and sevoflurane on rat ventricular cells and investigated the role of the sarcoplasmic reticulum (SR) in these inotropic actions. Single ventricular myocytes, isolated from rat hearts, were stimulated electrically at 1 Hz and contractions recorded optically. Cells were exposed to a range of concentrations of halothane, isoflurane or sevoflurane for a period of 1 min to determine the concentration-dependency of their inotropic actions. For each anaesthetic, the peak negative inotropic action was determined early during an exposure, and sustained negative inotropic action was measured at steady-state just before wash-off. In some experiments, cells were equilibrated with ryanodine 1 mumol litre-1 to investigate the role of the SR in these intropic effects. Halothane caused a concentration-dependent initial increase in contractions (to mean 130 (SEM 28)% at 10 mmol litre-1) followed by rapid onset of a negative inotropic effect (K0.5 0.34 mmol litre-1 for peak effect; K0.5 0.46 mmol litre-1 for sustained effect). Exposure to isoflurane induced a small potentiation of contractions in some cells, followed by a concentration-dependent decrease in contraction in all cells (K0.5 0.85 mmol litre-1 for peak effect; K0.5 1.92 mmol litre-1 for sustained effect); contractions recovered partially during a 1-min exposure. On wash-off, contractions were increased transiently above control. Sevoflurane caused a large initial decrease in contraction which then returned rapidly towards control (K0.5 0.2 mmol litre-1 for peak effect; K0.5 2.57 mmol litre-1 for sustained effect). In common with isoflurane, removal of sevoflurane caused a transient increase in contractions above control. After exposure to ryanodine, the positive inotropic effects of halothane and isoflurane did not occur, and recovery of contractions during exposure to isoflurane and sevoflurane was abolished as was the transient increase in contractions seen on wash-off, indicating that these effects were mediated via the SR. Halothane had the most potent sustained negative inotropic effect but there was little difference between the negative inotropic effects of isoflurane and sevoflurane at clinically relevant concentrations. At higher concentrations, sevoflurane caused a less potent negative inotropic effect than isoflurane. The SR plays a major role in the effects of all three anaesthetics. One possible mechanism underlying the initial potentiation of contraction by halothane (and isoflurane) may be sensitization of the Ca(2+)-induced Ca(2+)-release process of the SR.

Anesthetics, Inhalation↗

PubMed2002

Role of nitric oxide and cyclooxygenase pathways in the coronary vascular effects of halothane, isoflurane and desflurane in red blood cell-perfused isolated rabbit hearts.

BACKGROUND: The coronary vascular endothelium could mediate some of the coronary effects of halogenated anaesthetic agents. The role of the endothelial vasodilator substances nitric oxide (NO) and prostaglandins (PGs) in the coronary effects of halothane and isoflurane remains to be determined and has not been investigated for desflurane. In this study, the roles of NO and cyclooxygenase pathways in the coronary effects of halothane, isoflurane and desflurane were studied in isolated red blood cell-perfused rabbit hearts. METHODS: Rabbit hearts were perfused by a Langendorf technique with red blood cells mixed with modified Krebs-Henseleit buffer. Coronary blood flow (CBF), oxygen consumption and myocardial performance were evaluated during exposure to 0.5, 1 and 2 rabbit minimum alveolar concentrations of halothane, desflurane and isoflurane. Thereafter, the same protocol was applied with the addition of N(G)-nitro-L-arginine (L-NNA), indomethacin or a combination of both inhibitors. RESULTS: Similar and significant increases in CBF were observed with increasing concentrations of isoflurane and desflurane. In contrast, CBF did not change with halothane. The combination of the two antagonists abolished desflurane-induced vasodilation, whereas it did not change the isoflurane-mediated increase in CBF. Halothane-induced vasoconstriction was observed in the presence of a combination of indomethacin with L-NNA. CONCLUSIONS: Halothane and desflurane induce the release of vasodilating prostaglandins and NO in rabbit coronary arteries. In contrast, these mediators are not involved in the coronary vasodilating properties of isoflurane.

Anesthetics, Inhalation↗

PubMed2002

Phenotyping malignant hyperthermia susceptibility by measuring halothane-induced changes in myoplasmic calcium concentration in cultured human skeletal muscle cells.

BACKGROUND: Malignant hyperthermia (MH) is a potentially lethal disease triggered by volatile anaesthetics and succinylcholine in genetically predisposed individuals. Because of the heterogenetic nature of MH, a simple genetic-based diagnostic test is not feasible and diagnosis requires an invasive open muscle biopsy followed by the in vitro contracture test (IVCT). Our aim was to establish if measurements of halothane-induced increases in intracellular calcium ion concentration [Ca(2+)](i) in cultured human skeletal muscle cells can be used to phenotype MH susceptibility and if different mutations in the ryanodine receptor (RYR1) gene affect halothane-induced increases in [Ca(2+)](i). METHODS: Primary cultures of human skeletal muscle cells were established from 54 individuals diagnosed by the IVCT according to the protocol of the European MH Group as: MH susceptible (n=22), MH negative (n=18) or MH equivocal (n=14). All individuals were screened for the presence of the most common mutations in the RYR1 gene. [Ca(2+)](i) was measured by fluorescent digital microscopy using fura-2/AM in 10 cells from each patient at five different halothane concentrations. RESULTS: The halothane-induced increase in [Ca(2+)](i) differed significantly between the three diagnostic groups. Different mutations of the RYR1 gene did not have a specific impact on halothane-induced increases in [Ca(2+)](i). CONCLUSIONS: Measurements of [Ca(2+)](i) in human skeletal muscle cells can be used to phenotype MH susceptibility; however, we did not observe a specific effect of any mutation in the RYR1 gene on the halothane-induced increase in [Ca(2+)](i).

Adolescent↗

PubMed2003

Blood/gas partition coefficients of halothane, isoflurane and sevoflurane in horse blood.

BACKGROUND: Blood/gas partition coefficients (lambda(b/g)) for volatile agents in horse blood are reported for halothane but not for isoflurane and sevoflurane. We measured the lambda(b/g) of halothane, isoflurane and sevoflurane in the blood of fasted horses. The correlation with age, weight and some haematological and biochemical variables was studied. The temperature correction factor for isoflurane solubility was calculated. METHODS: Twenty-four horses were randomly allocated to halothane (n=8), isoflurane (n=8) or sevoflurane (n=8). Blood samples were taken after 10 h' fasting. Calculation of lambda(b/g) was based on the measurement of anaesthetic partial pressures in blood at 37 degrees C, which was achieved with tonometer equilibration and headspace gas chromatography. RESULTS: Mean lambda(b/g) was 1.66 (SD 0.06) for halothane, 0.92 (0.04) for isoflurane, and 0.47 (0.03) for sevoflurane. The lambda(b/g) values were all significantly lower than in humans (P<0.001). No correlation was found between lambda(b/g) and weight, age, haematocrit, plasma triglycerides, cholesterol or total bilirubin. The change in isoflurane solubility per 1 degrees C temperature increase was -2.63 (0.13)%. CONCLUSION: The lambda(b/g) values of halothane, isoflurane and sevoflurane in fasted horses are significantly lower than those reported in humans. The lambda(b/g) for halothane in this study agrees with values reported in the literature but a positive correlation with plasma triglycerides could not be confirmed. Knowledge of lambda(b/g) can refine models of anaesthetic uptake.

Anesthetics, Inhalation↗

PubMed2005

Halothane enhances dopamine metabolism at presynaptic sites in a calcium-independent manner in rat striatum.

BACKGROUND: We have previously reported that halothane anaesthesia increases the extracellular concentration of dopamine (DA) metabolites in the rat striatum with no change in DA. Although the metabolism of catecholamines is a source of oxidative stress, there is little information about DA metabolism and anaesthesia. We assessed the mechanism(s) of enhanced DA metabolism induced by halothane. METHODS: Microdialysis probes were implanted into male Sprague-Dawley rats and perfused with artificial cerebrospinal fluid (CSF). The dialysate was injected directly into an HPLC every 20 min. Each group of rats (n=5-7) was administered saline, apomorphine 100 microg kg(-1), pargyline 7.5 or 75 mg kg(-1), reserpine 2 mg kg(-1) or alpha-methyl-p-tyrosine (AMPT) 250 mg kg(-1). Another set of rats was perfused with artificial CSF containing tetrodotoxin (TTX) 1 microM or calcium-free CSF containing 10 mM EGTA. Rats were anaesthetized with halothane 0.5 or 1.5% 1 h after pharmacological treatments. RESULTS: In rats pretreated with apomorphine, despite a decrease in DA concentration, halothane induced a increase in DA metabolites. Pargyline (high dose) and reserpine completely and AMPT partially antagonized the increase in DA metabolites induced by halothane anaesthesia. TTX perfusion reduced the increase in DA, whereas calcium-free CSF perfusion did not. CONCLUSIONS: Our data suggest that halothane accelerates DA metabolism at presynaptic sites by releasing DA from reserpine-sensitive storage vesicles to the cytoplasm in a calcium-independent manner. The metabolic oxidative stress of inhalation anaesthesia requires future investigation.

Adrenergic Uptake Inhibitors↗

PubMed1982

The Ca-releasing action of halothane on fragmented sarcoplasmic reticulum.

Ca-releasing action of halothane on fragmented sarcoplasmic reticulum (FSR) from bullfrog and rabbit skeletal muscle was examined to understand the mechanism of Ca release in reference to the etiology of malignant hyperthermia. Halothane has dual action on FSR: the Ca release and the inhibition of Ca uptake. On addition of halothane to loaded FSR, a rapid Ca release was followed by a sluggish Ca leakage which was probably due to a decreased capacity for Ca uptake. The properties of the rapid Ca release by halothane are similar to those of caffeine. It was inhibited by procaine or high concentrations of Mg2+. It was stimulated by a high concentration of ATP. A low temperature was stimulatory for Ca-releasing action on frog FSR while it was inhibitory on rabbit FSR. The result that caffeine shifted the dose response curve for Ca release by halothane to a steeper relation to a range of much lower concentrations suggests that the action of halothane may not be identical with that of caffeine in spite of many similarities.

Adenosine Triphosphate↗