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PubMed1985

Associations between marker genotypes, halothane reaction, creatine kinase activity and meat quality characters in a sample of German Landrace pigs.

Routine blood typing of German Landrace pedigree populations and an earlier study revealed very low frequencies of the favourable alleles at the marker loci Phi, Pgd and H. The hypothesis was that in this population the whole linkage group of favourable alleles at the halothane and neighbouring marker loci may have been lost as a consequence of intense selection for leanness and type. The present study of 1050 German Landrace pigs at the Relliehausen experimental station, where some effort has been made to maintain a higher frequency of the favourable alleles PhiA (0.48), H- (0.43) and PgdA (0.70) gave quite different results. The frequency of halothane-positive pigs found by using a severe test was only 30%. Only 5.4%, 8.8%, 13.4% and 13.9% of animals with PhiA/A, H-/-, PgdA/A and PhiA/B genotypes respecitively were halothane-positive. Forty to sixty per cent of pigs with these marker genotypes could therefore be expected to be homozygous halothane-negative (N/N) animals. Creatine kinase activity and three selected meat quality characters showed highly significant differences between the A/A and the B/B genotypes for the marker loci Phi and Pgd, with the heterozygotes being intermediate. These differences are greater than those observed between halothane-negative and halothane-positive phenotypes. The only other consistently superior marker genotype in this population was the H blood group genotype H-/-. In contrast to findings from Sweden and Switzerland, the postalbumin locus Po2 and the suppressor locus S for the A-O blood groups did not exhibit useful marker qualities.(ABSTRACT TRUNCATED AT 250 WORDS)

Alleles↗
PubMed1991

Thiamylal- and halothane-sparing effect of diazepam in dogs.

The thiamylal- and halothane-sparing effect of diazepam was studied in two experiments using 32 conditioned dogs. Twenty-four dogs received 0.05, 0.1 or 0.2 ml/kg diazepam or 0.9% saline (placebo) prior to the administration of thiamylal sodium i.v. Eight dogs received 0.1 or 0.2 mg/kg diazepam i.v. or placebo prior to or during halothane anesthesia. All three doses of diazepam significantly decreased the amount of thiamylal required to allow orotracheal intubation. The 0.2 mg/kg i.v. dose of diazepam produced the most significant effects. Premedication of dogs with diazepam did not reduce the concentration of halothane required to maintain anesthesia. The administration of 0.1 and 0.2 mg/kg diazepam i.v. during halothane anesthesia decreased the concentration of halothane required to maintain anesthesia. These studies demonstrate that diazepam reduces the amount of thiamylal required for orotracheal intubation, and when given intra-operatively reduces the concentration of halothane required to maintain anesthesia.

Animals↗
PubMed1978

Operating room nurses' psychomotor and driving skills after occupational exposure to halothane and nitrous oxide.

Concentrations of halothane and nitrous oxide were assayed by gas chromatography throughout a working day in three operating theatres and in the end-tidal air of 19 nurses 15 and 60 min after leaving the theatres. Perceptual, psychomotor and driving skills were measured in these nurses and in 11 younger nurses working in the wards of the same hospital. A complicated psychomotor test battery and a driving simulator were used. End-tidal air concentrations of halothane and nitrous oxide were positively correlated with the exposure level of these gases in the operating theatres. Some of the operating room nurses had greater amounts of halothane in their end-tidal air (average 15 to 10 ppm) than student volunteers 4.5 h after 3.5 min of general anaesthesia with a combination of halothanenitrous-oxide oxygen (10 ppm halothane). These volunteers had worse psychomotor and driving performances when measured than controls who had not been anaesthetized. No correlations were found between the concentrations of halothane or nitrous oxide in end-tidal air and psychomotor or driving performance. Despite their higher age and exposure to the operating room environment, the driving skills of the operating room nurses were similar to those of the ward nurses. The results suggest that tolerance to anaesthetic gases develops among operating room personnel. No impairment of driving skills can be expected after daily exposure to halothan and nitrous oxide among long-term employees in operating theatres.

Air Pollutants↗
PubMed1979

Comparative effects of repeated and prolonged inhalation exposure of beagle dogs and Cynomolgus monkeys to anaesthetic and subanaesthetic concentrations of enflurane and halothane.

Male and female Beagle dogs and Cynomolgus monkeys were exposed to anaesthetic (1.5 MAC) and subanaesthetic (1/100 MAC) levels of enflurane and halothane for 3 hours on alternate days for 4 weeks. One-half of the animals were killed following the last exposure and the remainder after 4 weeks of recovery. The animals' condition was assessed during anaesthetic periods by measuring respiration, ECG, blood pressure, temperature and EEG. Haematology, urinalysis and clinical chemistry parameters were evaluated. Gross and microscopic pathological examinations were conducted at the end of the exposure and recovery periods. Two female monkeys in the mid- and high-dose halothane groups died during the study. No deaths were observed in the enflurane group. No quantitative differences were observed in respiration rate, heart rate, blood pressure and EEG activity of animals anaesthetized with enflurane or halothane. Muscle twitches were observed in some mid- and high-dose dogs inhaling enflurane, but not in monkeys. A number of liver function tests became abnormal in mid- and high-dose halothane-treated dogs and high-dose halothane-treated monkeys. This was not observed with enflurane. Histopathologic alterations were confined to the liver of animals exposed to halothane. In dogs, the lesions were characterized by centrilobular hepatocyte degeneration and/or necrosis, fibroblastic proliferation, hepatocyte enlargement, fat deposition and glycogen depletion; and in mid- and high-dose monkeys by moderate to marked hepatocyte vacuolation and fat deposition. Except for one high-dose dog, these lesions were not seen in animals killed after 4 weeks of recovery. No histopathologic alterations were observed with enflurane.

Alanine Transaminase↗
PubMed1980

Heart rate-systemic blood pressure relationship in dogs during halothane anesthesia.

We have quantified the sensitivity and range of response of baroreflex-mediated heart rate changes during halothane anesthesia. Anesthesia was induced in 10 dogs with sodium thiopental (4 mg/kg i.v.), morphine sulfate (1 mg/kg), and succinylcholine (0.5 mg/min) was infused. After instrumentation, we infused sodium nitroprusside (0.1 mg/ml) or gave phenylephrine in divided doses (0.05 mg i.v.) at end-tidal halothane concentrations of 0.5%, 1.0%, and 2.0%. We changed systolic pressure over the range 6.5-26 kPa, measuring systolic pressure and heart rate responses at 1.3-2.6 kPa intervals. We found that the sigmoid curve relating heart period and systolic pressure was displaced leftwards, and the range of reflex response was significantly depressed (P < 0.001) at 2% halothane concentrations. The maximum slope of the curve was significantly depressed (P < 0.001) at increasing halothane concentrations. We conclude that halothane depresses the slope of the relationship between blood pressure and heart rate. However, the reflex response range is only depressed at high halothane concentrations, and the curve is displaced in the direction of lower heart rates at any given systemic pressure.

Anesthesia, Inhalation↗
PubMed1981

Hepatic gluconeogenesis during halothane anaesthesia in man.

It is known that hepatic gluconeogenesis from lactate and aminoacids is inhibited by halothane in in vitro studies on isolated, perfused livers. In the present work, the effect of halothane anaesthesia on hepatic gluconeogenesis was studied in three volunteers during a constant amino-acid infusion and compared with three control subjects who did not receive any halothane during the amino-acid infusion. Prior to the investigation, all the subjects were on a carbohydrate-poor diet in order to deplete hepatic glucogen stores. During the investigation, hepatic gluconeogenesis was stimulated by a constant amino-acid infusion which caused a slight rise in total hepatic blood flow (THBF), a marked increase in splanchnic oxygen consumption and oxygen extraction, elevation in blood glucose and urea levels and in splanchnic glucose and urea releases. Halothane anaesthesia administered during continued amino-acid infusion caused a reduction in THBF to sub-control values, while the increased oxygen consumption was only slightly reduced, thereby further increasing splanchnic oxygen extraction. Blood glucose and urea levels of the anaesthetized subjects were consistent with those of the control subjects. Splanchnic release of glucose was reduced almost to control values during halothane. However, the release of urea was only slightly reduced. It is concluded that the stimulating effect on hepatic gluconeogenesis caused by the amino-acid infusion was inhibited during halothane anaesthesia, while metabolization of the amino-acids, other than through gluconeogenesis, proceeded without any major changes.

Adult↗
PubMed1982

Effects of halothane on coronary haemodynamics and myocardial metabolism in patients with ischaemic heart disease and heart failure.

Halothane was administered at an end-tidal concentration of 1% to 10 patients with stable ischaemic heart disease and clinical and haemodymanic signs of moderate heart failure. Measurements of central haemodynamic variables, coronary sinus blood flow and oxygen, lactate and hypoxanthine balances over the myocardium were done before and at steady state during halothane anaesthesia. Halothane induced marked haemodynamic changes with decreases in mean arterial pressure (-43%), mean pulmonary arteriolar occlusion pressure (-42%), systemic vascular resistance (-31%), cardiac index (-20%) stoke volume index (-31%) and left and right stroke work indices (-62% and -55%, respectively). Heart rate and pulmonary vascular resistance did not change. Coronary sinus blood flow decreased in parallel with perfusion pressure, and myocardial oxygen consumption decreased (-40%), as did myocardial oxygen extraction. Rate pressure product and triple product correlated better with changes in myocardial oxygen consumption in the present subset of patients than in healthy volunteers during halothane anaesthesia. The findings suggest that halothane, through its systemic vasodilatory effect, unloads the failing left ventricle and that this peripheral action predominates over the direct cardiodepressant action of the agent. The combined findings of unchanged coronary vascular resistance, decreased myocardial oxygen extraction and absence of increasing or pathological levels of lactate and hypoxanthine in coronary sinus blood imply a direct dilatory effect of halothane on the coronary vasculature.

Aged↗
PubMed1982

The role of halothane and fentanyl in the production of balanced anaesthesia.

The aim of the study was to quantitate the degree of respiratory depression when tolerance of superficial nociception and of an endotracheal tube was achieved by supplementing N2O + O2 anaesthesia either with halothane alone or with halothane in combination with fentanyl. Eighty-four patients, matched into seven groups, were studied after induction of anaesthesia with thiopental (4 mg/kg) and suxamethonium (3 mg/kg) using the following supplementation: 0.8, 0.6, 0.4% halothane alone or 0.4, 0.2, 0% halothane with 0.5-2 micrograms/kg fentanyl. After 10 min administration of the anaesthetic mixture using manual intermittent positive pressure ventilation (IPPV) (end-tidal CO2 c. 5.5%), IPPV was discontinued and spontaneous respiration allowed to return. When the end-tidal CO2 had stabilized, samples for blood gas analysis were taken and superficial antinociception was tested by pinching an inguinal skin fold. Supplementation of an N2O + O2 mixture with 0.8% halothane without fentanyl or with 0.4% halothane with 0.5 microgram/kg fentanyl seemed to come closest to the optimum in producing tolerance of an endotracheal tube and of superficial nociception (in about 85% of cases with an increase in PCO2 to only 7 kPa.

Adult↗
PubMed1984

Catecholamine and endocrine response in children during halothane and enflurane anaesthesia for adenoidectomy.

In 28 children undergoing adenoidectomy, plasma concentrations of catecholamines, ACTH and cortisol were measured. Fourteen children were anaesthetized with halothane (seven non-intubated, seven intubated) and 14 with enflurane (seven non-intubated, seven intubated). During undisturbed anaesthesia, plasma catecholamines were significantly higher with halothane than with enflurane (P less than 0.05). Immediately after surgery, catecholamines were increased up to 300% in the halothane groups. In the enflurane groups, however, the catecholamine concentrations remained unchanged. This difference between the two agents, after surgery, was statistically significant (P less than 0.01 for intubated and P less than 0.001 for non-intubated children). Fifteen minutes postoperatively no difference was found in plasma concentrations between the groups. In all four groups, plasma concentrations of ACTH and cortisol increased similarly during the procedure. It was concluded that plasma catecholamines were higher during halothane than during enflurane anaesthesia in children undergoing adenoidectomy. This difference may be caused by a stimulating effect of halothane on the endogenous catecholamine release. This increased sympathomimetic response during halothane anaesthesia was correlated to the incidence of ventricular arrhythmias previously found with this agent during adenoidectomy.

Adenoidectomy↗
PubMed1984

Intravenous infusion of halothane dissolved in fat. Haemodynamic effects in dogs.

Eight harrier dogs received an i.v. infusion of halothane dissolved 1:9 in a fat emulsion for i.v. nutrition (Intralipid, Vitrum). The rate of infusion was adjusted to maintain end-tidal halothane concentrations of 0.7% and 1.4%. At 1.4%, mean arterial pressure decreased to 76 +/- 8 mmHg (10.1 +/- 1.0 kPa) (mean +/- s.e.mean) from a pre-infusion value of 122 +/- 6 mmHg (16.2 +/- 0.8 kPa) (P less than 0.01). The concomitant decrease in cardiac output was 39% and left ventricular maximum dp/dt decreased by 50% (P less than 0.01). Changes in systemic vascular resistance and pulmonary arterial pressure were small. The haemodynamic responses during halothane inhalation, to corresponding end-tidal concentrations, were similar. Arterial and mixed venous halothane concentration increased in proportion to end-tidal concentration. There were no changes in arterial PO2 during the halothane-in-fat infusion. Triglyceride concentrations in plasma increased 12-fold. Haemodynamic recovery after the infusion was fast. We conclude that the halothane-in-fat infusion caused a dose-dependent depression of myocardial contractility and arterial pressure, similar to that seen during inhalation, and that end-tidal concentration could be used for control of the infusion rate.

Anesthesia, Intravenous↗
PubMed1989

Relationship between changes in power spectra of electroencephalograms and arterial halothane concentration in infants.

A power spectral analysis of electroencephalograms (EEGs) was performed in 30 infants who underwent plastic surgery for cleft lip or cleft palate. The study was conducted to investigate whether there was a significant correlation between EEG changes and arterial halothane concentration in infants. The power spectral analysis of EEGs was performed by the fast Fourier transform (FFT). Arterial halothane concentration was measured with gas chromatography. The relationship between the changes in the power spectra of EEGs and the arterial halothane concentration was examined by means of a multivariate analysis. Prior to administration of halothane, two kinds of EEG patterns were discernible. In one pattern the peak of the EEG power spectra was seen in the slow wave band (slow wave group); in the other the peak of the power spectra was present in the fast wave band (fast wave group). In the occipital lead the multiple correlation coefficient and the index of determination of the slow wave group were 0.71 and 0.50, respectively, and those of the fast wave group were 0.78 and 0.61, respectively. A significant correlation was proved to be present between the normalized values of the EEG power spectra and arterial halothane concentration in the occipital lead. Therefore, the results of the present study suggest that the relationship between changes in the power spectra of EEGs in the occipital lead and arterial halothane concentration in infants can be expressed by means of multiple regression formulas.

Anesthesia, Inhalation↗
PubMed1994

Inhibitory effects of halothane on high(K+)-induced canine tracheal smooth muscle contraction and intracellular Ca2+ increment.

Halothane is a potent bronchodilator. The effects of halothane on isolated canine tracheal smooth muscle contraction and intracellular Ca(2+) increment induced by a high concentration of K+ were investigated to clarify how this anaesthetic decreases intracellular Ca2+ concentration ([Ca2+]i), an important second messenger. The tension of the muscle strips was measured using an isometric transducer, and [Ca2+]i was measured using a surface fluorescence spectroscopy. Exposure to a 72.7 mM K+ solution increased muscle tension and [Ca2+]i. Halothane (1,2,3 and 4% at the vaporiser) was introduced by bubbling in the presence of the 72.7 mM K+, and significantly decreased both this elevated muscle tension and the [Ca2+]i in a concentration-dependent manner. Similarly, slowly decreasing concentrations of K+ (48.5, 36.4, 24.2 and 18.2 mM) significantly decreased both of these variables. There was no significant difference between the slopes of the two regression lines of changes in muscle tension and changes in [Ca2+]i. From the evidence that tonic increase in [Ca2+]i by high concentrations of K+ is due to the influx of Ca2+ via L-type voltage channels, halothane may modify the L-type channels to decrease Ca2+ influx. In conclusion, halothane inhibits the high K(+)-induced canine airway smooth muscle contraction by decreasing [Ca2+]i. The decrease in [Ca2+]i by halothane might be due to inhibition of voltage-operated channels, especially the L-type channels.

Animals↗
PubMed1995

Sevoflurane for ENT-surgery in children. A comparison with halothane.

Sevoflurane, a new volatile anesthetic agent, is of great potential interest in pediatric anesthesia. Its use for ENT surgery in children was compared with halothane in this study. Altogether 40 children participated in the investigation. In 18 (median age 4.2 years), halothane was used. The remainder (median age 4.0 years) were anesthetized with sevoflurane. After rectal premedication with midazolam and atropine, anesthesia was induced by mask (the agent in O2/N2O, 40/60) using a Mapleson D system. The trachea was intubated without the use of muscle relaxants and the children were then allowed to breathe spontaneously at fresh gas flows set high enough to avoid rebreathing. Hemoglobine oxygen saturation (SpO2), inspired and expired gas concentrations, respiratory rate (RR), heart rate (HR), ECG and blood pressure were followed. Equianesthetic concentrations of the agents were used and induction characteristics were comparable between the two agents. RR and end-tidal CO2 tensions were similar in the two groups. HR and systolic blood pressures were, however, higher with sevoflurane. Cardiac arrhythmias were seen more frequently with halothane (61%) than with sevoflurane (5%). During emergence, postoperative nausea/vomiting was more frequent after halothane anesthesia. Initially, postoperative excitement occurred more often after sevoflurane, when paracetamol was given during anesthesia, which was reduced (P < 0.01) when paracetamol was given at the time for premedication. It is concluded that sevoflurane is an excellent induction agent, and maintains heart rate and systolic blood pressure better than when halothane is used. The incidence of cardiac arrhythmia is lower with sevoflurane than with halothane.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoidectomy↗
PubMed1995

Caffeine-halothane accuracy in MH testing.

The accuracy and stability of caffeine and halothane concentrations in liquid Krebs medium were examined. Caffeine-Krebs Ringer's solution in incremental concentrations from 0.25 to 10 mM (N = 8 for each concentration) was serially assayed over a three-year period. Storage was at 4 degrees C. For serial testing of halothane during a five month period, halothane 1% or 3% in carbogen was bubbled through a Krebs solution, contained in muscle baths, either using a roller pump (to eliminate vaporizer back pressure) or using carbogen at a line pressure of 4-6 lbs/in2 (27-41 kPa). Halothane in Krebs was assayed by high pressure liquid chromatography. Caffeine concentrations did not vary for 20 weeks. From then, through 60 weeks, concentrations less than 2 mM steadily diminished; after that, through 156 weeks, only 4, 8, and 10 mM were stable. When compared to the halothane concentration in gas entering the muscle baths, halothane concentration in Krebs was predictable regardless of method delivery, as long as a gas analyzer indicated the proper concentration. We conclude that caffeine solutions are stable for 20 weeks when refrigerated, and for three years at concentrations 4 mM or greater.

Caffeine↗
PubMed1997

alpha 1-adrenoceptor stimulation is able to reverse halothane-induced cardiac depression in isolated rat hearts.

BACKGROUND: Stimulation of myocardial alpha 1-adrenoceptors has been shown to exert positive inotropic effects through a cyclic AMP-independent mechanism. The purpose of this study was to examine if alpha 1-adrenoceptor stimulation is able to attenuate myocardial depression produced by exposure to halothane, and to test if alpha 1-adrenoceptor stimulation alters myocardial oxygen supply-demand balance in hearts exposed to halothane. METHODS: The effects of phenylephrine were examined in 7 isolated perfused rat hearts. Variables measured were: heart rate, isovolumetric peak left ventricular pressure (LVP), LV dP/dt, coronary arterial flow, myocardial O2 delivery (DO2), myocardial O2 consumption (MVO2) and the ratio of DO2/MVO2. Each heart was exposed to phenylephrine cumulatively 0.1 microM, 0.3 microM, 1 microM and 3 microM under the administration of 1% halothane in the presence of propranolol 1 microM. RESULTS: Halothane 1% decreased the heart rate by 9 +/- 3%, LVP by 37 +/- 3%, and LV dP/dt by 35 +/- 2%. Phenylephrine restored these decreases to the baseline levels. Phenylephrine maintained or further enhanced the reductions in coronary flow and DO2 produced by halothane, resulting in a decrease in the DO2/ MVO2 ratio. CONCLUSION: alpha 1-adrenoceptor stimulation is capable of restoring direct cardiac depressant effects of halothane with a possible impairment of the oxygen supply-demand balance.

Anesthetics, Inhalation↗
PubMed2005

Intrathecal picrotoxin minimally alters electro-encephalographic responses to noxious stimulation during halothane and isoflurane anesthesia.

BACKGROUND: Isoflurane and halothane act in the spinal cord to blunt ascending transmission of impulses to the brain resulting from noxious stimulation. Because intrathecal picrotoxin (an antagonist at the gamma-aminobutyric acid-A receptor) partially reverses the immobilizing effect of isoflurane and halothane, we hypothesized that the electroencephalographic response to noxious stimulation would likewise be partially reversed by intrathecal picrotoxin. METHODS: Rats were anesthetized with isoflurane (n = 8) or halothane (n = 8) and a laminectomy performed. Following determination of minimum alveolar concentration (MAC), the electroencephalogram (EEG) was recorded during separate applications of a hindpaw clamp, tail clamp and electrical current to the tail at 0.8 and 1.2 MAC. Picrotoxin was then applied to the exposed spinal cord and the EEG response to noxious stimulation again determined. RESULTS: The EEG was more active during halothane anesthesia than isoflurane (spectral edge frequency for 95% power: 25.6 +/- 2.1 Hz vs. 23.1 +/- 1.6 Hz, P < 0.05). Noxious stimulation usually caused the EEG to shift to higher frequencies (e.g. for 0.8 MAC halothane, median edge frequency for 50% power: from 7.6 +/- 3.1 Hz to 10.7 +/- 2.6 Hz, P < 0.05). Picrotoxin minimally affected this response. CONCLUSIONS: Noxious stimulation evokes an EEG response that is minimally altered by intrathecal picrotoxin. This suggests that isoflurane and halothane do not have GABAergic actions in the spinal cord that indirectly suppress the EEG response.

Anesthetics, Inhalation↗
PubMed2005

Bispectral Index values are higher during halothane vs. sevoflurane anesthesia in children, but not in infants.

BACKGROUND: Previously, we have shown in adult patients that bispectral index score (BIS) values are significantly higher during halothane anesthesia (53-61 units) as compared with those observed during equipotent concentrations of sevoflurane (39-43 units). Because halothane is frequently used in the pediatric setting, we tested the hypothesis that BIS values observed in children might also be higher during general anesthesia with halothane than with sevoflurane. METHODS: Forty-one healthy, unpremedicated pediatric patients scheduled for elective operations received either halothane or sevoflurane titrated as appropriate for surgical stimulation. RESULTS: During maintenance sevoflurane anesthesia (n=20), the mean BIS values and percent end-tidal concentrations were 44+/-14 and 2.1+/-0.6, respectively, whereas for the halothane group (n=21) the corresponding values were 61+/-7 and 1.1+/-0.4, respectively. CONCLUSION: These findings suggest that BIS values are higher during halothane vs. sevoflurane anesthesia in children, but not in infants.

Age Factors↗
PubMed1975

The mechanism of the halothane-dependent efflux of calcium from rat-liver mitochondria.

The halothane-dependent, calcium-induced loss of respiratory control in rat liver mitochondria [1, 2] is Mg2plus -dependent and is accompanied by an enhanced mitochondrial swelling. It is suggested that this swelling reflects an increase in calcium activity in the matrix space, due to a decrease in binding of the accumulated cation. This change in the partition of intramitochondrial calcium is correlated with an inhibition by halothane of energy-independent, calcium-induced swelling. The enhanced swelling associated with the active accumulation of calcium in the presence of halothane does not lead to a marked increase in permeability to other ions. Nevertheless, under conditions of energised calcium uptake, and in the presence of Mg2plus, a halothane-dependent, ruthenium red-insensitive efflux of calcium is observed. This is consistent with the proposed halothane-dependent increase in the matrix activity of accumulated Ca2plus. It is suggested that this mechanism accounts for the previously postulated [2] futile cycle of calcium uptake and release induced by halothane in rat liver mitochondria.

Animals↗