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Results for “Halothane”

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At least 19 recordsLinked to original sources
PubMed1977

Anaesthesia for Caesarean section. Analysis of blood concentrations of halothane using 0.2% or 0.65% halothane with 50% nitrous oxide in oxygen.

In 15 patients anaesthesia for elective Caesarean section was maintained with 50% nitrous oxide in oxygen and a 0.65% halothane supplement. In a further 15 mothers a 0.2% halothane supplement was used. In those mothers receiving 0.65% halothane intermittent measurements were made of maternal arterial halothane concentrations during the uptake and the excretion of the agent. At delivery the foetal umbilical venous concentrations were measured also. The mean time between administering halothane and delivery was 10.5 min (SD 3.5). The mean maternal arterial halothane concentration at delivery was 6.03 mg/100 ml (SD 0.75) and the mean umbilical vein concentration was 2.13 mg/100 ml (SD 0.69). The regression of Apgar scores at 1 min after delivery on umbilical vein halothane concentration at delivery was not significant. In the mothers receiving 0.2% halothane measurements of halothane concentration were made in five patients only. The mean maternal arterial halothane concentration at delivery was 1.56 mg/100 ml (SD 0.52) and the mean umbilical vein and artery concentrations were 0.8 and 0.38 mg/100 ml respectively. The use of 0.2% and 0.65% halothane supplements prevented awareness in all the mothers. However, dreaming occurred in two patients given a 0.2% halothane supplement. Studies are required to establish the minimum halothane supplement required to prevent awareness in a larger series of patients.

Adolescent↗
PubMed1977

Halothane macrophage migration inhibtiion factor test in halothane-associated hepatitis.

As an index of delayed hypersensitivity in vitro halothane macrophage migration inhibition factor tests (halothane-MIF tests) were performed on peripheral blood lymphocytes from five patients with halothane hepatitis. Twenty-two subjects exposed to halothane, but with no evidence of jaundice, five 'healthy' hospital anaesthetists, nine jaundiced subjects without halothane exposure, and 10 healthy subjects with no history of exposure to halothane were also tested. The halothane-MIF test was positive in four of the five patients with halothane-induced hepatitis; the negative result was in a patient on steroid treatment. The test was negative in all other subjects. Our findings suggest that the halothane-MIF test may be of value in the diagnosis of halothane-induced hepatitis and as a screeening procedure for the identification of susceptible subjects.

Adult↗
PubMed1976

Hypoxia and halothane metabolism in vivo: release of inorganic fluoride and halothane metabolite binding to cellular constituents.

Fluoride release and covalent binding of halothane metabolites were studied in rats pretreated with phenobarbital and anesthestized with halothane in the presence of high (40 per cent) and low (7 per cent) oxygen tensions. The purpose of producing hypoxia was to promote the reductive pathways involved in the metabolism of halothane. Halothane anesthesia under hypoxic conditions caused a significant elevation in the plasma fluoride concentration. There was also a greater than three-fold increase in covalent binding of 14C-halothane metabolites to microsomal lipids in hypoxic rats. The lipid/protein binding ratio in control animals averaged 0.76, while hypoxic animals had a binding ratio of 3.24. The findings demonstrate that defluorination of halothane does occur during hypoxic conditions. It is hypothesized that the products produced by this reductive metabolic pathway are also potentially more hepatotoxic than the oxidative metabolites, based upon the increased covalent binding of halothane metabolites under hypoxic conditions.

Animals↗
PubMed1978

Sensitisation to halothane-altered liver components in severe hepatic necrosis after halothane anaesthesia.

In-vitro sensitisation (inhibiton or stimulation of leucocyte migration) in response to a liver homogenate obtained from rabbits pretreated with halothane was found in eight of twelve patients with halothane-associated hepatitis. Sensitisation was not observed when the homogenates were obtained from animals pretreated with ether. Furthermore, leucocyte migration in response to "halothane homogenate" was normal in eleven patients who had shown no abnormality in liver function after halothane anaesthesia and in thirty patients with other liver diseases. These studies provide direct evidence that sensitisation to halothane-altered liver-cell components is present in those occasional patients in whom severe liver damage develops after halothane anaesthesia.

Adult↗
PubMed1977

A study of the mechanism of halothane-induced liver necrosis. Role of covalent binding of halothane metabolites to liver proteins in the rat.

Various anesthetic and nonanesthetic doses of [1-14C]halothane were administered separately to normal and phenobarbital-pretreated (PBP) rats by ip route. The rats were sacrificed at 0.5-24 h after dosing, and livers were removed and examined histopathologically for tissue necrosis. Only PBP rats that received anesthetic doses of halothane (11.5 or 23 mmol/kg) and sacrificed 24 h after dosing exhibited liver toxicity. Determination of the radioactivity distribution among various liver macromolecules revealed that the protein fraction contained the highest activity at all time points in all animals. The lipid fraction showed some radioactivity during the initial 1-6 h period which disappeared after 6-8 h, while the DNA fraction was devoid of radioactivity in all animals injected with [14C]halothane. All the PBP rats that exhibited liver necrosis consistently attained higher covalent binding of halothane metabolites to liver proteins (2.13-2.20 nmol/mg of protein) when compared with the protein binding (1.12-1.41 nmol/mg of protein) observed among the rats that did not exhibit liver toxicity during the same time period. These results suggest a correlation between covalent binding of halothane metabolites to liver proteins and halothane-induced liver necrosis.

Alanine Transaminase↗
PubMedDate not supplied

Anaerobic release of fluoride from halothane. Relationship to the binding of halothane metabolites to hepatic cellular constituents.

Halothane has been found to undergo a reductive defluorination. This reaction requires an active cytochrome P-450 system and NADPH, and is inducible by phenobarbital and polychlorinated biphenyls but not by methylcholanthrene. The fluoride release occurs only under low O2 tension, while high O2 tension results in the oxidation of halothane to trifluoroacetic acid, inorganic bromide, and chloride. The release of the inorganic fluoride is linear up to 60 min. Because the conditions required for fluoride release and the binding of a halothane metabolite to microsomal phospholipids are similar, the defluorinated halothane molecule is assumed to be involved with this binding. However, based on the amount of fluoride released, the defluorinated halothane metabolite represents only approximately 60% of the total amount of halothane metabolite bound, which suggests that more than one metabolite may be involved in the binding.

Aerobiosis↗
PubMed1992

In vivo muscle 31P nuclear magnetic resonance spectroscopy during treatment of halothane-sensitive and halothane-nonsensitive pigs.

In vivo muscle 31P nuclear magnetic resonance spectroscopy was performed on 10 female pigs originating from a homozygous halothane-sensitive line and on 10 female pigs from a homozygous halothane-nonsensitive line. The mean concentration of phosphocreatine in the biceps femoris muscle of the anesthetized pigs decreased to 86% of the initial value after 11 minutes of halothane exposure (3%, oxygen flow 3 L/min). After the next 5.6 minutes, phosphocreatine concentration reached a minimal value of 52%, followed by a mean recovery to 76% of the initial value during the ensuing 11 minutes. Response was not observed in anesthetized homozygous halothane-nonsensitive pigs. Thus, a decrease to 86% of the initial value of phosphocreatine was 100% predictive for homozygous halothane-sensitive pigs with body weight ranging from 10 to 18 kg.

Adenosine Triphosphate↗
PubMed1992

Thermoregulatory thresholds for vasoconstriction in pediatric patients anesthetized with halothane or halothane and caudal bupivacaine.

The thermoregulatory threshold for vasoconstriction has been studied in infants and children given isoflurane, but not in those given halothane anesthesia. More importantly, the effect of vasoconstriction on central temperature in pediatric patients remains unknown. Also unknown is the effect of caudal analgesia on vasoconstriction thresholds. Accordingly, in the first portion of this study, we determined the central thermoregulatory threshold in 23 infants and children given approximately 0.6% halothane and caudal anesthesia for abdominal surgery. Patients were prospectively assigned to one of four weight groups: 5-10, 10-20, 20-30, and 30-50 kg. The threshold was considered the central temperature triggering peripheral vasoconstriction, and significant vasoconstriction was defined as a forearm-fingertip skin-surface temperature gradient exceeding 4 degrees C. Thresholds were similar (approximately 35.7 degrees C) in each study group, suggesting that thermoregulatory responses to halothane anesthesia are similar in infants and children of differing weights. However, they were higher than expected based on the previously reported thresholds in pediatric patients given isoflurane anesthesia. After peripheral vasoconstriction, central temperature continued to decrease in patients weighing more than 30 kg but remained constant or increased slightly in the others. These data suggest that thermoregulatory responses are more effective in infants and small children than in bigger children or adults. In the second part of this study we evaluated the effect of caudal analgesia on the thermoregulatory threshold for vasoconstriction. Children undergoing hypospadias repair were anesthetized with halothane (0.9%) and oxygen. Following induction, they were randomly assigned to caudal analgesia (n = 7) or penile nerve block (n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Caudal↗
PubMed1977

Adiposity and the pharmacokinetics of halothane. The effect of adiposity on the maintenance of and recovery from halothane anaesthesia.

Thirty fit patients (15-70 years, 46-98 kg) undergoing body-surface operations were selected to include a wide range of adiposity (12-45% of total body weight estimated from measurements of skinfold thickness). They were anaesthetized with halothane and 70% N2O in O2. From measurements of total ventilation (ml min-1 kg-1) and of halothane concentrations in inspired (F1) end-tidal (FE') and 'mixed-spill' (FS) gases, the following parameters were calculated for 5-min intervals from 20 to 40 min after induction; the rate of uptake of halothane per percent inspired concentration (Vha1 ml min-1%-1) and the degree of equilibrium achieved with the inspired concentration, calculated as FE'/F1 expressed as a percentage. Multiple-regression analysis of the results for 19 patients, taking account of the effects of body fat, ventilation, age, and the blood-gas partition coefficient lambda of halothane for the individual patient, showed that Vha1 increased with adiposity (b=0-375, P=0-0019), and with ventilation (b=0-054, P=0-09) but decreased with increasing age (b=-0-258, P=0-006). The time intervals between the end of the anaesthetic and the achievement of four defined levels of recovery (response to painful stimulus obedience to a simple command, response to a question, orientation in time and space), were recorded. Multiple-regression analysis showed that recovery time increased with addiposity, duration of administration and end-tidal concentration at the end of the administration, and decreased with increasing age. All four effects were statistically non-significant at the first levels of recovery but all increased at the later levels and all eventually became significant.

Adolescent↗
PubMed1975

Circulatory effects of halothane and halothane-nitrous oxide anesthesia in the dog: spontaneous ventilation.

The cardiovascular effects of equipotent (minimum alveolar concentration; MAC) doses of halothane versus halothane plus 25% N2O (H25N2O) in spontaneously breathing dogs do not differe except that nitrous oxide increased mean arterial pressure (AP) and decreased arterial oxygen partial pressure (PAO2). When 75% nitrous oxide was added to halothane anesthesia, AP, mean pulmonary artery pressure (PAP), heart rate (HR), cardiac output (CO), stroke volume (SV), total peripheral resistance (TPR), and left ventricular work (LVW) increased and PAO2 and hemoglobin saturation decreased. Arterial oxygen tensions below 80 torr were common at moderate and deep anesthetic levels of halothane plus 75% N2O (H75N2O). The specific contribution of N2O, hypoxemia, hypercapnia, or temporal recovery (or a combination of these) in producing cardiovascular stimulation were not determined.

Anesthesia, Inhalation↗
PubMedDate not supplied

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

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

Animals↗
PubMed1976

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

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

Bromides↗
PubMed1977

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

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

Adult↗
PubMed1992

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

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

Anesthesia, Inhalation↗
PubMed1976

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

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

Anesthesia, Inhalation↗