PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Halothane”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

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↗
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↗
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↗
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↗
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↗
PubMed1976

Inhibition of catecholamine release from the adrenal medulla by halothane. Site and mechanism of action.

In isolated bovine adrenals perfused with Locke solution in a retrograde fashion we investigated the effects of halothane on the catecholamine release evoked by various secretagogues. 1. The catecholamine release induced by activation of the nicotinic receptors on the chromaffin cells with 1,1-dimethyl-4-phenylpiperazinium was almost completely inhibited (by about 90%) by 1.4 X 10(-3) M halothane. 2. It was shown by means of cumulative concentration-response curves of acetylcholine for its stimulating effect on catecholamine release (pD2 = 4.04) that halothane was a non-competitive antagonist (pD'2 = 3.17). 3. Halothane (1.4 X 10(-3) and 4.3 X 10(-3) M) did not decrease the catecholamine secretion in response to pilocarpine or histamine. 4. The 5-hydroxytryptamine-induced catecholamine release was not impaired by 1.4 X 10(-3) M halothane, but was significantly inhibited (by 44%) by 4.3 X 10(-3) M halothane. 5. At 1.4 X 10(-3) M halothane the catecholamine release induced by gamma-aminobutyric acid (GABA) was inhibited by 40%. 4.3 X 10(-3) M halothane completely blocked the secretion induced by GABA. 6. The catecholamine secretion in response to 56 mM KCl or to introduction of CaCl2 after perfusion with Locke solution deficient in CaCl2 was not reduced by halothane (1.4 X 10(-3) and 1.4 X 10(-2) M). 7. Halothane (1.4 X 10(-3) M) did not inhibit the catecholamine release evoked by acetaldehyde or tyramine from glands perfused with Ca2+ -free Locke solution throughout the experiments. It is concluded that the site of action of halothane is the cell membrane of the chromaffin cell. The anaesthetic does not impair the permeability of the membrane to calcium ions. Halothane may cause a conformational change of membrane proteins, particularly of the nicotinic receptor (and at higher concentrations of GABA and 5-hydroxytryptamine receptors); thus, stimulation may be prevented by an inhibition of agonist-receptor interaction.

Acetaldehyde↗
PubMed1975

The effects of halothane on hepatic microsomal electron transfer.

1. The effects of halothane (CF3CHBrCl), a volatile anaesthetic agent, on electron transfer in isolated rat liver microsomal preparations were examined. 2. At halothane concentrations achieved in tissues during clinical anaesthesia (1-2mM), halothane shifts the redox equilibrium of microsomal cytochrome b5 in the presence of NADPH towards the oxidized form. Halothane accelerates stoicheiometric consumption of NADPH and O2, increases the rate of reoxidation of NADH-reduced microsomal ferrocytochrom b5, but does not affect NADPH- or NADH-cytochrome c reductase activity. The enhanced microsomal electron flow seen in the presence of halothane is not diminished by CO nor is it increased by pretreatment of the animals with phenobarbital. 3. The effects of halothane are maximum in microsomal preparations isolated from animals fed on a high-carbohydrate diet to induce stearate desaturase activity. Changes in microsomal electron transfer caused by halothane are in all cases abolished by low concentrations (1-2mM) of cyanide. Microsomal stearate desaturase activity is unaffected by halothane. 4. The first-order rate constant for oxidation of membrane-bound ferrocytochrome b5 in the absence of added substrate (k1 equals 1.5 times 10(-3)A-1) is similar to that for autoxidation of purified ferrocytochrome b5(k1 equals 7 times 10(-3)S-1) the rate of autoxidation of soluble ferrocytochrome b5 is unaffected by halothane. 5. It is concluded that the effects of halothane on microsomal electron transfer are not related to cytochrome P-450 linked metabolism but rather arise from the interaction of halothane with the cyanide-sensitive factor of the stearate desaturase pathway.

Animals↗
PubMed1975

Halothane and isometric contractions of isolated pregnant rat myometrium.

The effects of halothane on isometirc contractions of isolated pregnant uterine muscle strips were evaluated in tissue obtained from 13 midpregnant rats. Peak developed tension was depressed in a dose-related manner at halothane concentrations above 0.8 vol per cent, but was not affected at lower halothane concentrations. Time to peak tension was reduced 10-20 per cent, and relaxation time, 10 per cent, by halothane concentrations ranging up to 2.2 per cent. Total resting tension consisted of a passive component and a calcium-dependent component. In concentrations above 0.8 per cent, halothane rapidly removed 100 per cent of the calcium-dependent resting tension. At lower concentrations, halothane reduced it 50 per cent. The passive component of resting tension was unaffected by halothane. These actions of halothane can prevent postpartum hemostasis. They occur even with very low anesthetic concentrations and can be detected soon after introduction of anesthetic into the muscle bath. This indicates that the hemostatic hazards associated with the use of halothane for delivery may not be prevented by limiting the concentration of halothane or the duration of anesthetic exposure.

Anesthesia, Obstetrical↗