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PubMed1984

Liver damage after halothane anaesthesia: analysis of cases in Finnish hospitals in 1972-1981.

A retrospective questionnaire revealed 11 patients with halothane related liver disturbances in Finland in 1972-1981. Seven of the cases were regarded as obvious and two as probable halothane hepatitis (HH). Four patients suffered HH twice, and none of the cases had a fatal outcome. The speed of onset of icterus correlated with the number of halothane exposures, as did the increase in liver enzyme (ASAT, ALAT) activities and the increase in serum bilirubin concentration. Halothane anaesthesia is strictly contraindicated if a nondefinite icterus has appeared after a previous exposure to halothane. It should not be given if unclear fever or prolonged nausea have followed a previous exposure. No major adverse effects or organ toxicity connected with enflurane were found.

Adult↗
PubMed1980

Compared effects of enflurane and of halothane on the intracranial pressure and the cerebral perfusion pressure in the dog.

In this study, we compare the values of the systemic arterial pressure (S.A.P.), of the intracranial pressure (I.C.P.) and of the cerebral perfusion pressure (C.P.P.) -- (C.P.P. = P.A.S. -- I.C.P.) -- in the anesthetized dog, artificially ventilated, before and after vaporization with two halogenated anesthetics, enflurane and halothane at different concentrations. The measures were made in a group of ten dogs in normoventilation and intracranial normotension conditions, in one hypercapnic dog with intracranial hypertension, and in four dogs after injection of sodium laurylsulfate in the internal carotide to induce cerebral edema. In normocapnic dogs, enflurane and halothane increase the I.C.P., decrease the S.A.P. and the C.P.P. Under enflurane 0.5%, the I.C.P., the S.A.P., and the C.P.P. show no significant variations. The increase in I.C.P. is due to the cerebral vasodilator effect of the anesthetics. At equal concentrations, halothane is more hypotensive than enflurane, and the changes in C.P.P. induced by both anesthetics depend more on the variations in S.A.P. than on the variations in I.C.P. In the hypercapnic dog, the vaporization of enflurane and of halothane further enhance the increase in I.C.P., since the vasodilator effect of the anesthetics is added to that of hypercapnia. The S.A.P. and the C.P.P. drop in relation to the concentrations of vaporization used. After sodium laurylsulfate, the administration of enflurane and halothane is accompanied by a drop in S.A.P. and in C.P.P. In this group, the decrease in I.C.P. recorded in two thirds of the cases can be explained by the hypotensive effect of the anesthetics which decreased the hydrostatic pressure in the cerebral vascular bed, a maintenance element of the edema.

Anesthesia, Inhalation↗
PubMed1983

Effects of halothane and fentanyl on the rate of CSF production in dogs.

Using the open ventriculocisternal perfusion method, the rate of cerebrospinal fluid (CSF) production was examined in dogs anesthetized with either halothane (0.8%) or fentanyl (3.0 micrograms/kg/min for 20 min, then 0.2 micrograms/kg/min, intravenously), and nitrous oxide (60-70%) in oxygen. Halothane decreased the mean rate of CSF production from 0.047 +/- 0.006 ml/min (mean +/- SEM) in controls to 0.033 +/- 0.005 ml/min. This effect persisted throughout 3.0-3.5 h of anesthesia. When the expired concentration of halothane was decreased from 0.8% to less than 0.1%, the mean rate of CSF production returned to control values within 45-50 min. Fentanyl produced no change in the mean rate of CSF production compared to controls. These data suggest that increased CSF volume does not contribute to increased intracranial pressure during prolonged halothane anesthesia. In patients at risk for increased intracranial pressure due to increased CSF volume, either halothane or fentanyl may be preferable to anesthetics that may increase CSF production, e.g., enflurane.

Absorption↗
PubMed1980

Mechanical properties of normal and malignant hyperthemia susceptible porcine muscle: effects of halothane and other drugs.

Malignant hyperthemia, which can be initiated in susceptible humans and swine by the volatile anesthetic halothane, appears to result from abnormal responses in skeletal muscle. We have inferred the primary defect in susceptible muscles by observing their responses to certain drugs. Furthermore, we compared the responses of cut muscle cell preparations, such as those used in the diagnostic caffeine test, with those of intact muscle cells. Specifically, we investigated the effects of halothane, caffeine, succinylcholine and catecholamines on the mechanical properties of intact muscle cells from normal pigs, mice and frogs and susceptible pigs. The results from intact and paired cut cell preparations were qualitatively similar. Halothane (2%) caused a 30% decrease in peak tetanic tension in susceptible porcine muscle but less than a 10% change in other muscles. Halothane potentiated twitch tension in frog and susceptible pig muscle. The latter was 4 times more sensitive to caffeine twitch potentiation than normal muscle. Porcine intercostal muscles were more sensitive to caffeine than limb extensor muscles and the difference between normal and susceptible muscle was less with intercostal muscles. Succinylcholine and catecholamines had small and opposite effects on porcine muscles; when used together in combination with halothane there was little effect on normal muscle but a dramatic decrease in tetanic tension and rapid onset of contracture in susceptible muscle.

Animals↗
PubMed1980

Contribution of asynergic contraction to halothane-induced myocardial depression.

We investigated the possibility that myocardial asynergy (dyscoordinate contraction) is a contributing mechanism to the impairment of cardiac function produced by halothane. Coronary cineangiograms were performed in seven dogs, awake and at 1, 2, and 3 MAC halothane. The relative motions between four arterial bifurcations (six segments) were plotted as an indication of changing ventricular dimensions. To quantitate ventricular asynergy, we calculated anisotropy (AI) and asynchrony (AS), the coefficient of variation of mean shortening (S-) and of mean time to half shortening (T-50), respectively, of the six segments. From these a myocardial performance index (MPI) was derived: MPI = S-/AI + T-50 + AS. In general, S- and MPI decreased with increasing halothane concentration. Anisotropy showed a trend, although usually insignificant, toward increasing, while AS did not change. These observations have two implications. First, asynergy of contraction contributes little, if anything, to halothane-induced impairment of myocardial performance. Second, changes in measurements of intact cardiac performance, such as dP/dtmax, may be reasonably valid during halothane, provided loading conditions are taken into account.

Anesthesia, Inhalation↗
PubMed1980

A halothane-induced biochemical defect in muscle of normal and malignant hyperthermia-susceptible Landrace pigs.

Muscle adenosine triphosphate (ATP), glucose-6-phosphate, phosphocreatine, and pH were measured in nine malignant hyperthermia (MH)-susceptible and 14 MH-resistant Landrace pigs. Muscle biopsies were taken before (under barbiturate anesthesia) and after exposure to halothane. When compared to levels during barbiturate anesthesia, exposure to halothane had no immediate effect on muscle ATP levels in either MH-susceptible or -resistant pigs. However, once malignant hyperthermia developed in susceptibe pigs ATP levels decreased significantly. In both susceptible and resistant pigs halothane increased muscle glucose-6-phosphate and decreased muscle phosphocreatine and pH significantly below control levels observed during barbiturate anesthesia. In susceptible pigs these changes were significantly more marked than were the changes produced in resistant pigs. These data indicate that the effect of halothane on muscle metabolism is similar in both MH-resistant and -susceptible pigs. The results suggest that the effect of halothane is to inhibit aerobic metabolism by preventing mitochondrial dehydrogenation of pyruvate. Inhibition is complete in susceptible pigs but only retarded in resistant pigs. In susceptible pigs the consequent lactacidosis, hyperthermia, and reduction in ATP synthesis contribute to the development and maintenance of rigidity.

Adenosine Triphosphate↗
PubMed1980

In vivo changes in canine ventricular cardiac conduction during halothane anesthesia.

Changes in the ventricular conduction system associated with halothane anesthesia were investigated by direct methods of His bundle recording, pacing, and premature stimulation in a canine model. In eight animals a change from 1.5% to 2.4% halothane concentrations was associated with significant prolongation of epicardial activation times by an average of 2.4 and 2.9 msec during atrial and His bundle paced rhythms, respectively. Ventricular functional refractory periods decreased significantly by an average of 7.3 msec, the effective refractory period of the ventricular conduction system did not system did not change, and epicardial conduction delays at the effective refractory period decreased. In six other animals the addition of 1.5% halothane to basal thipental anesthesia was not associated with prolongation of epicardial activation times or decreased ventricular functional refractory periods. However, the effective refractory period of the ventricular conduction system significantly decreased by an average of 9.1 msec, and epicardial conduction delays at the effective refractory period significantly increased by an average of 9.6 msec. A change in halothane concentrations from 1.5% to 2.4% is associated with depression of ventricular conduction and shortened duration of refractory periods in the ventricular conduction system in vivo in a manner consistent with the reported actions of halothane on Purkinje fibers in vitro.

Anesthesia↗
PubMed1981

Characteristics of succinylcholine-produced phase II neuromuscular block during enflurane, halothane, and fentanyl anesthesia.

The characteristics of phase II neuromuscular block following repeated intravenous injections of succinylcholine (SCh) were determined in 15 adult patients during enflurane, halothane, or fentanyl-nitrous oxide anesthesia. The onset of phase II block (train-of-four ratio (T4) equal to 0.5) occurred following a cumulative SCh dose of 4.4 +/- 0.3 (SEM) mg/kg of enflurane, 5.1 +/- 0.5 mg/kg of halothane, or 6.4 +/- 0.5 mg/kg of fentanyl. The cumulative SCh dose producing phase II block during fentanyl-nitrous oxide anesthesia was significantly greater than during enflurane (p less than 0.01) or halothane (p less than 0.05) anesthesia. Based on these data it is predicted that the likelihood of phase II block developing is less during fentanyl administration than during enflurane or halothane anesthesia. An abrupt transition from phase I to phase II neuromuscular block, as evidenced by an accelerated decrease in the T4 ratio, was observed during enflurane or halothane anesthesia as the cumulative SCh dose approached 3 to 5 mg/kg. The transition phase was delayed during fentanyl-nitrous oxide anesthesia, occurring after a cumulative SCh dose of 4 to 7 mg/kg. Following this transition, tachyphylaxis (decreased time between SCh injections) was observed in each study group. The T4 ratio in all three study groups stabilized at 0.15 to 0.25 after 7 to 8 mg/kg.

Adult↗
PubMed1981

Halothane-induced cardiac arrhythmias following administration of aminophylline in experimental animals.

Cardiac arrhythmias often occur when patients receiving aminophylline are anesthetized with halothane. This animal study was designed to define what constitute arrhythmogenic doses of aminophylline when administered before halothane anesthesia. One group of six dogs was given aminophylline, 10 mg/kg IV, followed in 3 minutes by inhalation of 1% halothane. In two additional groups of dogs the same experimental protocols were used except that aminophylline doses were 25 mg/kg and 50 mg/kg. In the first group, two of six dogs developed ventricular arrhythmias during induction of halothane anesthesia. One of six dogs given 25 mg/kg of aminophylline developed a ventricular arrhythmia. Three of six dogs given 50 mg/kg of aminophylline developed ventricular arrhythmias. Sustained ventricular arrhythmias occurred in 33% of the animals with "therapeutic" serum theophylline levels and in 33% of the animals with "toxic" levels. Induction of halothane anesthesia within 15 minutes of aminophylline administration may be dangerous and is likely to result in severe and persistent ventricular arrhythmias.

Aminophylline↗
PubMed1982

Cardiovascular depression during halothane anesthesia in infants: study of three induction techniques.

Hemodynamic changes during three techniques for induction of halothane anesthesia were studied in 90 healthy infants aged 5 to 26 weeks who were randomly divided into three groups of 30 patients each. In group I, anesthesia was induced using halothane in concentrations that were increased to 3%. In group II, atropine, 0.02 mg/kg, was given intramuscularly before induction, followed by induction as in group I. In group III, halothane in concentrations that were increased to 1.25% was followed by intramuscular succinylcholine, 2 mg/kg, 90 seconds after the start of induction. In all three groups N2O 3 L/min and O2 2 L/min were employed using a non-rebreathing system. Heart rate (HR) and blood pressure (BP) were recorded at 1-minute intervals for 20 minutes. HR decreased 30% in group I, 18% in group II (p less than 0.01), and 29% in group III. BP decreased 50% in group I (p less than 0.01), 34% in group II, and 33% in group III. During halothane induction in infants, bradycardia can be minimized with preoperative atropine; the degree of hypotension can be diminished with either preoperative atropine or the use of intramuscular succinylcholine combined with lower concentrations of halothane.

Anesthesia, Inhalation↗
PubMed1982

Effect of halothane on rested-state and potentiated-state contractions in rabbit papillary muscle: relationship to negative inotropic action.

The effect of halothane on the availability of different sources of activator calcium for myocardial contraction was evaluated in relationship to the negative inotropic effect on the anesthetic. This was studied in rabbit papillary muscle under various stimulation conditions that are known to vary the importance of one or another of two sources of Ca2+ for production of contraction. The rested-state contraction is known to depend primarily on the transsarcolemmal influx of Ca2+ for its activation whereas the potentiated-state contraction is dependent largely on Ca2+ released from intracellular stores. In the presence of 0.6% halothane (gas phase) the rested-state and potentiated-state contractions were depressed (mean +/- SEM) 38% +/- 5% (n = 15) and 32% +/- 3% (n = 7), respectively (no statistically significant difference). Halothane accelerated the decay of the potentiated state, indicating that it stimulates the loss of Ca2+ from internal stores. Halothane also acted to slow the time course of force increase following restimulation of rested muscles, indicating that it inhibits the filling of internal stores. These observations suggest that the negative inotropic effect of halothane is caused by a combination of quantitatively similar effects of the anesthetic on the transsarcolemmal and intracellular sources of activator Ca2+.

Animals↗
PubMed1981

[Halothane and spontaneous motility of human taenia libera in vitro (author's transl)].

Isolated human taenia libera shows spontaneous motility in the organ bath. The active basal tone, force development and frequency of spontaneous contractions and total power parameter "Montevideo Units" were first analysed under control conditions. Halothane lowered the active basal tone, frequency and the total power of the muscle strip in a dose-dependent manner. The amplitude and force of contraction of human taenia libera first began to increase under halothane, attaining its maximum at 1.0 vol.%. Halothane concentrations above 1.5 vol.% at first caused a depression and finally abolished spontaneous motility. The changes in the spontaneous motility pattern brought about by halothane were completely reversible. Possible causes for the halothane effect were considered as to the possible relevance to the in vivo situation.

Gastrointestinal Motility↗
PubMed1980

Time-course of formation of volatile reductive metabolites of halothane in humans and an animal model.

The time-course of the formation of 2-chloro-1,1,1-trifluoroethane (CTF) and 2-chloro-1-1-difluoroethylene (CDF), two recently identified volatile reductive metabolites of halothane, has been studied in four patients receiving 1% halothane with 99% oxygen. The concentrations of CTF and CDF in end-expired breath increased with time and reached a plateau after approximately 60 min from commencing administration. A similar time-course and plateau was seen when Fischer 344 rats were anaesthetized with halothane 1% in oxygen. However, there was an eight-fold and 12-fold increase in CTF and CDF concentrations respectively when halothane 1% was administered under conditions of mild hypoxia (oxygen 14% inspired) to rats pretreated with phenobarbitone (this results in a marked increase in serum alanine aminotransferase (ALT) and necrotic damage in the vicinity of the central veins of the liver). It is suggested that breath concentrations of CDF and CTF provide a sensitive method of monitoring the reductive metabolism of halothane.

Adult↗
PubMedDate not supplied

Influence of halothane on the level of enkephalins in discrete brain areas of rabbits.

With regard to the fact, that theory of anesthesia, based on the endogenous opioid peptides requires further investigations the aim of this paper was to measure the concentration of leucine- (LENK) or methionine-enkephalin (MENK) in discrete brain areas of rabbits during and after 1 h halothane (2% v/v) anesthesia. The level of LENK and MENK was measured in discrete brain areas using the radioimmunoassay. Animals were divided into the following groups, depending upon the duration of anesthesia: I-15 min; II-60 min; III-1 h after anesthesia termination; IV-control group of non-anesthetized animals. After halothane anesthesia evident decrease in the concentration of leu-enkephalins in hypothalamus (HT) and the opposite effect in hippocampus (H) were observed. The MENK level significantly increased after halothane (for 60 min) in hypothalamus, hippocampus and mesencephalon (M). The change in the level of LENK in the thalamus (Th), hippocampus and mesencephalon and in the level of MENK in the hypothalamus and mesencephalon persisted after withdrawal of anesthesia. It was found that the alterations in the level of enkephalins in discrete areas of rabbit's brain is a feature of halothane anesthesia. The explanation of this phenomenon is possibly important for the understanding of the mechanism of halothane anesthesia and requires further investigations.

Anesthesia↗
PubMed1993

Malignant hyperthermia: halothane- and calcium-induced calcium release in skeletal muscle.

The temperature dependence of oleic acid-enhanced halothane- induced Ca2+ release and the existence of a reduced threshold of Ca(2+)-induced Ca2+ release were examined to determine their roles in human malignant hyperthermia. Halothane (8-11 mM) induced Ca2+ release from terminal cisternae-containing preparations from skeletal muscle. Oleic acid (15 microM) markedly reduced the threshold of halothane-induced Ca2+ release to < 0.5 mM at 37 degrees C, but not at 25 degrees C, consistent with the temperature dependence of halothane action in intact muscle. Two states of the threshold of Ca(2+)-induced Ca2+ release were unrelated to malignant hyperthermia in humans, in contrast to pigs. Excess fatty acid production may be an important modulator of halothane action in malignant hyperthermia.

Animals↗
PubMedDate not supplied

Bupivacaine toxicity in lightly anesthetized pigs with respiratory imbalances plus or minus halothane.

BACKGROUND AND OBJECTIVES: Changes in acid base balance within the body, oxygen delivery to tissue, and carbon dioxide elimination, as well as general anesthetics, influence the toxicity of local anesthetics. The objective of this study was to test the hypothesis that light halothane anesthesia, hypercapnia, and hypoxia act together to alter the central nervous system and cardiovascular toxicity of bupivacaine. METHODS: Three groups of 2-week-old pigs were lightly anesthetized with N2O in O2 and paralyzed with pancuronium. One group (n = 6) was made hypercapnic (group A; PaCO2 > or = 60 mg Hg), another group (n = 6) was made hypercapnic and hypoxic (group B; F1O2 = 0.1, PaCO2 = 66.8 +/- 9.91 mm Hg, PaO2 = 29.2 +/- 3.53 mm Hg), and another group (group C; n = 5) was made hypercapnic and hypoxic and given 0.5% halothane (PaCO2 = 68.54 +/- 4.18, PaO2 = 31.06 +/- 1.96). Bupivacaine was infused intravenously at 1 mg.kg-1.min-1 until the animals developed cardiac asystole. RESULTS: Arrhythmias, seizures, isoelectric electroencephalogram (isoEEG), and asystole were readily identified in groups A and B. None of the animals given halothane had seizures, but they did exhibit the other three toxic endpoints. The doses of bupivacaine producing asystole were significantly less in group C than in group A (7.9 +/- 1.8 versus 17.7 +/- 2.2 mg.kg-1). The doses of bupivacaine that produced isoEEG were significantly lower in groups B and C than in group A (8.9 +/- 6.2, 5.0 +/- 1.1, 14.6 +/- 3.2 mg/kg, respectively). Doses of bupivacaine producing all toxic endpoints except seizures were lower in group B animals than in group A, but only the isoEEG doses were statistically different (arrhythmias 2.3 +/- 1.1 versus 3.7 +/- 1.1; isoEEG 8.9 +/- 6.2 versus 14.6 +/- 3.2; asystole 12.1 +/- 7.5 versus 17.7 +/- 2.2 mg.kg-1). No differences in seizure pattern or type of arrhythmia were detected. Mean arterial pressure decreased during bupivacaine infusion, the rate of decrease was fastest (P < .05) in the animals receiving halothane and slowest in the hypercapnic animals. Mean arterial pressure in group A increased significantly compared to control (to 135.5 +/- 14.4% of control; P < .01) before decreasing. Heart rate decreased and the differences over time among groups differed significantly. CONCLUSIONS: Bupivacaine is significantly more lethal, as judged by the doses producing asystole, in young pigs that are hypercapnic, hypoxic, and receiving halothane than in young pigs that are hypercapnic.

Anesthesia↗
PubMed1993

The thermoregulation of halothane versus isoflurane in humans receiving ophthalmological surgery.

Although suppression of thermoregulatory mechanisms during anaesthesia is generally assumed, the extent to which thermoregulation may be inactive is unknown. Twenty unpremedicated, ASA physical status class I patients (17 men and 3 women) scheduled for retinal detachment surgery were studied to evaluate the different changes of core and two skin-surface temperatures during halothane or isoflurane anaesthesia. Anaesthesia was induced by mask inhalation of halothane or isoflurane in nitrous oxide 70% and oxygen and was maintained by mechanical ventilation during surgery with halothane or isoflurane in nitrous oxide 50% and oxygen only. Core temperature (rectus) and skin-surface temperatures (forearm and fingertip) were measured during surgery using three separate thermometers (Y.S.I.: Yellow springs instrument Co., Inc. G541-211-Y01-33A0). Operating room temperatures were recorded in every case. Significant vasoconstriction was prospectively defined by a skin-surface temperature gradient between two sampling sites > or = 4 degrees C. The result indicated that there was no significant difference between core temperatures and skin-surface temperature gradients during halothane anaesthesia and isoflurane anaesthesia. However, three of the ten patients had their skin-surface temperature gradients > or = 4 degrees C in the halothane group. None of the ten patients had their skin-surface temperature gradients > or = 4 degrees C in the isoflurane group.

Adult↗
PubMed1994

[Liver transplantation in halothane-induced liver necrosis].

The risk for developing acute liver failure after halothane exposition was calculated between 1:8,000 and 1:36,000. The case report given on a 22 year old man with halothane-induced hepatic failure is unusual, because the typical risk factors as age over 40, female sex, obesity, and previous exposure to halothane were not present. Two days after exposure to halothane the patient suffered acute liver failure with severe coagulopathy (factor V = 5% activity), and encephalopathy grade IV complicated by renal failure and respiratory insufficiency. Maximal increases of enzymes in blood were AST 3900 U/L, ALT 2570 U/L, LDH 10600 U/L. After six days the patient underwent liver transplantation with complete anuria and instable circulation. Explanted liver showed massive necrosis (70% of parenchyma) and fatty changes. The liver transplant had immediately a good function and renal failure resolved within three days. In the follow-up of 3 1/2 years the patient suffered no further complications. Culturing the patient's lymphocytes in the lymphocyte transformation test a strong reaction could be detected with a stimulatory index of 20. Maximal proliferation was observed when lymphocytes were incubated with plasma metabolites of a volunteer drawn 120 minutes after anesthesia with halothane was started.

Adult↗