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PubMed1997

Sevoflurane or halothane anesthesia: can we tell the difference?

UNLABELLED: This study was performed to evaluate the ability of anesthesiologists to differentiate between sevoflurane, a newer, more expensive anesthetic, and halothane. A total of 113 assessments were made by 36 anesthesiologists on 58 children, aged 6 mo to 6 yr, scheduled for bilateral myringotomy and tube placement. All patients received midazolam (0.5 mg/kg per os) approximately 30 min before the induction of anesthesia. Sevoflurane or halothane was randomly selected for anesthetic induction and maintenance. The anesthesiologists, who were unaware of the anesthetic being used, were asked to identify the anesthetic based on clinical signs and to assess the quality of induction, speed of induction, and speed of emergence using a visual analog scale (VAS; minimum score = 0, maximum score = 100). The anesthesiologists correctly identified the anesthetic only 56.6% of the time. This was not significantly different from the 50% that would result from random guessing (P = 0.08). Further, there were no significant differences in VAS scores between the two groups. This study suggests that in premedicated pediatric patients undergoing brief surgical procedures, anesthesiologists cannot correctly differentiate between sevoflurane and halothane. The lack of significant differences in VAS scores suggests that the speed of induction, the speed of emergence, and the quality of induction are similar under these clinical conditions. Any purported benefits of sevoflurane seem to be of minor consequence under the circumstances studied. IMPLICATIONS: When the anesthetic halothane or sevoflurane is administered in a blind, randomized fashion, anesthesiologists could not reliably identify which drug was being used to anesthetize children for a brief surgical procedure. These results suggest that the differences between the two drugs in clinical practice are small and may not justify the additional cost of sevoflurane.

Anesthesia, Inhalation↗
PubMed1999

Halothane minimum alveolar anesthetic concentration and neuronal nitric oxide synthase activity of the dorsal horn and the locus ceruleus in rats.

UNLABELLED: There is some evidence of a relationship between nitric oxide and pain control pathways. However, it is still controversial whether nitric oxide synthase (NOS) inhibitors affect minimum alveolar anesthetic concentration (MAC). We examined the effects of 7-nitro indazole (7-NI), a selective neuronal NOS (nNOS) inhibitor, on halothane MAC. With nicotinamide adenine dinucleotide phosphate diaphorase histochemistry, we also investigated the nNOS activity of the dorsal horn and the locus ceruleus in 26 Sprague-Dawley rats. 7-NI (100, 500, 1000 mg/kg intraperitoneally) reduced halothane MAC to 0.34% +/- 0.12%, 0.1% +/- 0.03%, and 0.05% +/- 0.12%, dose dependently (P < 0.01). 7-NI also reduced the number of nicotinamide adenine dinucleotide phosphate diaphorase-positive cells by 20% to 65% (P < 0.05 or 0.01) and the staining intensity of the axons in the locus ceruleus and lumbar and thoracic spinal cord as compared with the control group. 7-NI reduced the MAC observed with halothane anesthesia, which was accompanied by nNOS activity suppression in the spinal cord and the locus ceruleus. Our results support the hypothesis that the nitric oxide signaling pathway is related to MAC. IMPLICATIONS: We examined the effects of a selective neuronal nitric oxide synthase inhibitor, 7-nitro indazole, on halothane minimum alveolar anesthetic concentration and measured the nitric oxide synthase activity in the spinal cord and the locus ceruleus of Sprague-Dawley rats using nicotinamide adenine dinucleotide phosphate diaphorase staining method. 7-Nitro indazole decreased both the minimum alveolar anesthetic concentration and neuronal nitric oxide synthase activity.

Anesthetics, Inhalation↗
PubMed2000

The hemodynamic effects of halothane and isoflurane in chick embryo.

UNLABELLED: The cardiovascular effects of volatile anesthetics in prenatal hearts are not well investigated. The purpose of this study was to determine whether the embryonic cardiovascular system is sensitive to an exposure to clinically relevant, equipotent concentrations of halothane and isoflurane. Stage 24 (4-day-old) chick embryos were exposed to 0.09 and 0.16 mM of halothane and 0.17 and 0.29 mM of isoflurane. Dorsal aortic blood velocity was measured with a pulsed-Doppler velocity meter. Halothane, but not isoflurane, caused a significant decrease in cardiac stroke volume and maximum acceleration of blood (dV/dt(max)), an index of cardiac performance. This effect was reversible, and during washout, stroke volume and dV/dt(max) increased above control levels. Embryonic heart rate was not affected by either drug. Chick and human embryos are similar during early stages of development; therefore, chick embryo may be a useful model to study the cardiovascular effects of anesthetics. IMPLICATIONS: In equipotent, clinically relevant concentrations, halothane, but not isoflurane, markedly decreased aortic blood flow and cardiac performance measured with ultrasound techniques in chick embryos. Chick and human embryos are similar during early stages of development; therefore, chick embryo may be a useful model to study the cardiovascular effects of anesthetics.

Anesthetics, Inhalation↗
PubMed2001

Blockage of one class of potassium channel alters the effectiveness of halothane in a brain circuit of Drosophila.

At concentrations comparable to those used in the clinic, halothane has profound effects on a neuronal pathway devoted to the escape reflex of the fruit fly, Drosophila melanogaster. We studied the influence of the potassium channel that is encoded by the Shaker gene on the halothane sensitivity of this circuit. Shaker channels were specifically inactivated either by genetic means, using strains with two different severe Shaker mutations, or by pharmacologic means, using ingestion of millimolar concentrations of 4-aminopyridine. In all cases, halothane potency decreased substantially. To ensure that the genetic alteration was specific, both mutations were studied as stocks that had been repeatedly backcrossed to a control strain. The specificity of the pharmacologic inhibition was demonstrated by the fact that 4-aminopyridine had no effect on halothane potency in a Shaker mutant. Quantitative differences in the effects of channel inhibition between males and females suggested a sexual dimorphism in the functional brain anatomy of the reflex circuit.

Anesthetics, Inhalation↗
PubMed2001

Oxygen and glucose deprivation-induced neuronal apoptosis is attenuated by halothane and isoflurane.

UNLABELLED: Both in vitro and in vivo evidence supports the reduction of early ischemic, both global and focal, brain injury by volatile anesthetics. However, the protection afforded by volatile anesthetics in later neuronal death, i.e., apoptosis, caused by global ischemia has not been investigated. We induced oxygen and glucose deprivation in neuronal cortical cell cultures prepared from newborn rats on in vitro Days 10-14. This hypoxic (PO2 <50 mm Hg) condition was maintained continuously (30, 60, and 90 min). In a separate experiment, the neuronal cell cultures were exposed to isoflurane (1.13%, 2.3%, or 3.3%) or halothane (1.7%, 3.4%, or 5.1%) before oxygen and glucose deprivation, with continued exposure to isoflurane or halothane during oxygen and glucose deprivation. After 48 h, neuronal apoptosis was assessed with terminal deoxynucleotidyl transferase-mediated in situ nick-end labeling and DNA gel electrophoresis. Oxygen and glucose deprivation (30, 60, and 90 min) caused significant apoptosis of cerebral cortical cultured neurons. However, pretreatment and continued treatment during the period of oxygen and glucose deprivation with halothane or isoflurane resulted in a concentration-dependent attenuation of oxygen and glucose deprivation-induced neuronal apoptosis. IMPLICATIONS: This is the first investigation to evaluate the effect of volatile anesthetics on oxygen and glucose deprivation-induced neuronal apoptosis. Oxygen and glucose deprivation-induced neuronal apoptosis can be decreased by prior and continued administration of halothane or isoflurane.

Anesthetics, Inhalation↗
PubMed1975

Interaction of ketamine and halothane in rats.

The interaction of intramuscularly injected ketamine and its N-demethylated metabolite (metabolite I) with halothane was evaluated in rats. Five, 10, 20, or 50 mg/kg of ketamine alone or 20, 50, or 100 mg/kg of metabolite I alone produced less than 10 minutes of hypnosis. However, halothane anesthetic requirement (i.e., MAC) was depressed in a dose-dependent fashion as much as 56% 1-2 hours and as much as 14% 5-6 hours after injection of ketamine, 50 mg/kg, im. The reduction in MAC was correlated with brain levels of ketamine or metabolite I, suggesting a ketamine:metabolite I potency ration of 3:1. The half-life of ketamine in plasma and brain was longer in the presence of halothane than when ketamine was given alone. It is concluded that ketamine is not a short-acting drug and that concomitant use with halothane would be expected to prolong further the duration of its action on the central nervous system.

Anesthesia, Inhalation↗
PubMed1975

The effects of halothane and enflurane on rat brain synaptosomal sodium-potassium-activated adenosine triphosphatase.

Synaptosomes, or nerve-ending particles, were isolated from the cerebral cortices of young rats by homogenization, differential centrifugation, and density-gradient centrifugation. The sodium-potassium-activated adenosine triphosphatase enzyme system [(Na+ plus K+)-ATPase] of these particles is believed to represent in vitro the sodium-potassium pump of the nerve terminal. Suspensions of synpatosomes were equilibrated with air containing various concentrations of halothane and enflurane, as determined by gas chromatography. Clinical concentrations of the anesthetics had no effect on (Na+ plus K+)-ATPase activity. Fourteen per cent halothane and 14.8 per cent enflurane in the gas phase resulted in 12 and 10 per cent inhibition, respectively, of (Na+ plus K+)-ATPase activity. These data confirm that interference with active cation transport by inhibition of neuronal (Na+ plus K+)-ATPase is not related to the mechanism of halothane or enflurane anesthesia. (Key words: Anesthetics, volatile, halothane; Anesthetics, volatile, enflurane; Metabolism, enzymes, ATPase; Nerve, synaptosomal ATPase; Theories of anesthesia, ATPase.).

Adenosine Triphosphate↗
PubMed1975

Anesthetic biotransformation and renal function in obese patients during and after methoxyflurane or halothane anesthesia.

Anesthetic biotransformation and renal function were studied in obese adult patients (148 plus or minus 8 kg; mean plus or minus SE) anesthetized for three hours with 60 per cent nitrous oxide plus either methoxyflurane or halothane for elective jejunoileal small-bowel-bypass operations. There was no evidence of persistent renal dysfunction in any patient postoperatively, but serum osmolality was elevated 72 hours after methoxyflurane anesthesia. Urine concentrating ability was not determined. Peak serum ionic fluoride concentration was 55.8 plus or minus 5.8 muM/1 two hours after discontinuation of methoxyflurane. Urinary ionic fluoride and oxalate excretions increased postoperatively. Compared with previously reported data from nonobese patients, serum ionic fluoride concentrations in obese patients increased more rapidly during methoxyflurane anesthesia and peaked higher and sooner after discontinuation of methoxyflurane. The peak serum ionic fluoride concentration was 10.4 plus or minus 1.5 muM/1 at the conclusion of halothane anesthesia, significantly more than the corresponding value in nonobese patients. Intraoperative liver biopsies from 23 of 27 patients showed moderate to severe fatty metamorphosis. Fatty liver infiltration may have increased hepatic anesthetic uptake and exposed more methoxyflurane or halothane to hepatic microsomal enzymes. The more rapid elevation and higher peak levels of serum ionic fluoride following methoxyflurane, and to a lesser extent following halothane, may reflect increased anesthetic biotransformation in obese compared with nonobese patients. To avoid excessive serum ionic fluoride elevations the authors recommended limiting low-dose methoxyflurane anesthesia delivered to obese patients with potential fatty liver infiltration to no more than three hours.

Adjuvants, Anesthesia↗
PubMed1975

Venomotor changes caused by halothane acting on the sympathetic nerves.

Experiments were performed to determine whether depression of venomotor responses with halothane results from interference with sympathetic activation or from an effect on venous smooth muscle cells. Changes in isometric tension of isolated canine saphenous-vein strips were recorded. Adrenergic activation was achieved by transmural electrical stimulation, by addition of tyramine, and by addition of morepinephrine. Halothane (0.5 to 3 per cent) did not significantly alter basal tension. It lessened the reaction of the veins to electrical stimulation but not their response to norepinephrine; it increased the response to tyramine. Since the responses to norepinephrine and tyramine were not decreased, halothane appears to act on the nerve terminal to prevent release of neurotransmitter associated with nerve-terminal depolarization. Thus, halothane causes inhibition of electrically induced venoconstriction in cutaneous veins, probably by interfering with the release of norepinephrine from nerve terminals rather than by an inhibitory effect on the smooth muscle cells.

Anesthesia, Inhalation↗
PubMed1976

Localization of molecular halothane in phospholipid bilayer model nerve membranes.

The molecular motion and distribution of the inhalation anesthetic halothane (2-bromo-2-chloro-1,1,1-trifluoroethane) in a phospholipid bilayer model nerve membrane preparation was studied using fluorine nuclear magnetic resonance. Bilayers containing stable free radicals at known depths were studied to measure possible localization of halothane within certain areas of the bilayer. Bilayer suspensions containing manganese ions in the aqueous phase were used to test the partition of halothane between the aqueous and lipid phases. It was found that halothane rapidly achieves complete exchange throughout the bilayer and the surrounding aqueous phase. The results provide experimental evidence against the formation of anesthetic clathrates hypothesized by Pauling and Miller in their theories of anesthesia.

Fluorides↗
PubMed1977

Recovery, psychomotor skills, and simulated driving after brief inhalational anesthesia with halothane or enflurane combined with nitrous oxide and oxygen.

Recovery from anesthesia was assessed in a controlled manner in 34 healthy student volunteers, using a psychomotor test battery 1 and 5 hours and a driving simulator 2, 4.5, and 7 hours after 3.5 minutes of anesthesia with halothane or enflurane combined with nitrous oxide and oxygen. Psychomotor performances remained significantly (P less than 0.05 to P less than 0.001) worse than in an unanesthetized control group for 5 hours after both halothane and enflurane. However, impairment of driving skills 4.5 hours after anesthesia was measurable only after halothane (P less than 0.05). It is concluded that after even brief periods of halothane or enflurane anesthesia patients should not drive or operate machinery for at least 7 hours. The magnitudes and durations of the residual effects of both agents on psychomotor performance were, however, less than those previously found after thiopental, methohexital, or diazepam.

Adult↗
PubMed1977

Halothane depresses baroreflex control of heart rate in man.

Baroreflex control of heart rate was determined during three awake control situations and during two depths of halothane anesthesia in man. Baroreflex function was quantiated by calculating the pressor test slope from the R-R interval change on the ECG produced by a pharmacologically induced pressor response. During the three awake control situations the subjects breathed room air or 100 per cent O2 spontaneously or 100 per cent O2 with ventilation controlled. Mean (+/- SD) slopes obtained were 15.1 +/- 4.5, 15.6 +/- 6.8 and 18.4 +/- 9.9, respectively. No significant difference in baroreflex function slope was observed. During light halothane anesthesia (0.7 per cent endtidal) baroreflex function was significantly depressed (mean slope = 2.5 +/- 1.5), and it was abolished at 1.1 per cent end-tidal halothane (mean slope = 0.03 +/- 0.04). It is concluded that halothane anesthesia produces depression of baroreflex control of heart rate in man.

Adult↗
PubMed1977

Canine systemic and cerebral effects of hypotension induced by hemorrhage, trimethaphan, halothane, or nitroprusside.

In 62 dogs, hypotension to a mean arterial pressure of either 40 or 50 torr (equivalent to a cerebral perfusion pressure of 30 or 40 torr, respectively) for one hour was induced by hemorrhage (oligemia), trimethaphan, halothane, or sodium nitroprusside. Before and during the period of hypotension, the following were measured: mean arterial blood pressure, cardiac output, whole-body O2 consumption, cerebral blood flow, cerebral O2 consumption, arterial blood gases, blood O2 content, and lactate, pyruvate, glucose, epinephrine, and norepinephrine concentrations. At the end of the period of hypotension, brain biopsies were taken for determination of adenosine triphosphate, phosphocreatine, lactate, and pyruvate concentrations. In an additional eight dogs following one hour of hypotension (at 40 torr) induced by one of the four techniques, the brains were perfused with carbon black, removed, and examined. In another ten dogs following hypotension (at 40 torr) induced with either halothane or trimethaphan, the animals were observed for three days and then killed for examination of the brain. Dogs maintained at a mean arterial pressure of 40 torr, despite differences in cerebral blood flow, demonstrated metabolic disturbances compatible with systemic and cerebral hypoxia. These were greatest in those dogs given nitroprusside in excess of 1.0 mg/kg, presumably due to cyanide toxicity. In dogs maintained at 50 torr, metabolic disturbances were minimal or absent in the halothane- and nitroprusside-treated dogs but were still apparent in the oligemic and trimethaphan-treated dogs. Carbon black infusions revealed no evidence of non-homogeneous flow. Three of the ten dogs observed for three days had persistent post-hypotension neurologic dysfunction. Two of these were given trimethaphan. The results suggest that the systemic and cerebral effects of halothane and nitroprusside (at doses less than 1.0 mg/kg) are similar and at a mean arterial pressure of 50 torr are of little consequence. By contrast, hypotension induced by trimethaphan or oligemia results in detectable metabolic alterations even at a pressure of 50 torr.

Adenosine Triphosphate↗
PubMed1977

Alteration by halothane of glucose and glycogen metabolism in rat skeletal muscle.

Exposure of resting rat diaphragm for one hour in vitro to halothane (1-1.5, 2-2.5 and 4-4.5 per cent in oxygen) produced significant alterations of intracellular glucose disposition. Glycolysis (as measured by lactate production) increased, while glycogen formation was inhibited in a dose-related fashion. Net glucose uptake was unaffected by the anesthetic except during exposure to 4-4.5 per cent halothane, when 14 per cent depression of uptake was found. Total glycogen content decreased, due mainly to the inhibition of glycogen synthesis and to some extent to a stimulation of glycogenolysis. The anesthetic did not interfere with the effect of insulin on glucose uptake or the intracellular disposition of glucose. Creatine phosphate concentrations decreased following exposure of diaphragm to 1-1.5, 2-2.5 and 4-4.5 per cent halothane, while the adenosine triphosphate concentration declined after exposure to 4-4.5 per cent only. Although the mechanism(s) whereby halothane alters glucose and glycogen metabolism are unknown, it is possible that the anesthetic acts primarily by affecting membranes containing enzymes involved in the metabolism of glycogen.

Adenosine Triphosphate↗
PubMed1977

Effects of halothane, thiopental, and lidocaine on fluidity of synaptic plasma membranes and artificial phospholipid membranes.

The effects of halothane, thiopental, and lidocaine were studied with spin-labeling methods in synaptic plasma membranes (order parameter) and artificial phospholipid membranes (lateral diffusion). Halothane had a biphasic action, low concentrations (0.64 mM) ordering and high concentrations (2.9 mM) fluidizing both types of membranes. A biphasic effect in phospholipid membranes was also seen with thiopental, 0.1 mM ordering and 10 mM fluidizing, whereas in synaptic plasma membranes both low and high concentrations caused an increased order in the lipid bilayer region. At high thiopental concentrations, a considerable number of molecules may have reacted with membrane proteins or accumulated in the highly fluidic hydrophobic interior region of the membrane without affecting the rotational movement of the labeled fatty acid. Lidocaine alone, or together with calcium chloride, at various concentrations to 10 mM had no significant effect, and a fluidizing effect of 1 mM calcium chloride was possibly a result of interaction of calcium chloride with the label. The results indicate that the three lipid-soluble anesthetics interact differently with the lipid part of membranes. Lidocaine did not seem to affect bilyer lipids, while thiopental and halothane in phospholipid vesicles and halothane alone in synaptic membranes caused a dose-dependent biphasic effect.

Anesthesia, Inhalation↗
PubMed1978

Responses to fasting and lipid infusion of epinephrine-induced arrhythmias during halothane anesthesia.

Sensitivities to epinephrine in fasted and non-fasted rats anesthetized with halothane or pentobarbital were determined. The arrhythmic threshold for epinephrine, i.e., the dose which upon injection produced four or more premature ventricular contractions, was significantly lower for 12-hour (5.5 +/- 3.2 microgram/kg), 24-hour (2.2 +/- 1.3 microgram/kg) and 48-hour (2.25 +/- 0.6 microgram/kg) fasted rats than for non-fasted rats (10.9 +/- 3.4 microgram/kg) at the same dose of halothane (2.0 per cent). Fasting had no effect on the arrhythmic threshold for epinephrine in rats anesthetized with pentobarbital (35 mg/kg). Infusion of a 10 per cent fatty acid emulsion caused a significant lowering of the arrhythmic threshold for epinephrine of fed rats, while infusion of acetoacetic acid had no effect on the arrhythmic threshold. It is concluded that the combination of fasting and halothane anesthesia renders the heart more sensitive to epinephrine than halothane anesthesia alone.

Anesthesia, General↗
PubMed1979

Lack of mutagenicity of two possible metabolites of halothane.

1,1-Difluoro-2-bromo-2-chloroethylene, a probable metabolite of halothane, was purified by preparative gas chromatography and tested for mutagenicity in the Salmonella/mammalian liver system developed by Ames and colleagues. 1,1,1-Trifluoro-2-chloroethane which had been isolated from the breath or rabbits anesthetized with halothane was also tested for mutagenicity in a similar manner. Both compounds were found to be nonmutagenic in this bacterial system. Although neither this study nor any other has yet been able to demonstrate that halothane or any of its metabolites is genetically active, nevertheless, unnecessary occupational exposure to the drug should be avoided due to the possibility that future studies could reveal adverse effects secondary to halothane.

Animals↗
PubMed1979

Indices of myocardial oxygenation during coronary-artery revascularization in man with morphine versus halothane anesthesia.

A prospective study in 12 adult male patients undergoing coronary-artery revascularization was conducted to compare the effects of a morphine versus a halothane anesthetic technique on several indices of myocardial oxygen supply and demand. Indices reflecting myocardial contractility, preload, afterload, and heart rate were measured. Undesirable increases in systemic and pulmonary capillary wedge pressure were minimized using sodium nitroprusside as needed. In the period after sternotomy but before revascularization, patients anesthetized with morphine (mean 2.1 mg/kg) had significant (P less than .05) increases in rate-pressure product, tension-time index, blood pressure, and heart rate, as well as relative myocardial ischemia, evidenced by significant ST-segment depression in the V5 lead of the EKG and a decreased diastolic pressure-time index/tension-time index compared with patients anesthetized with halothane (mean .75 per cent inspired). Few difficulties associated with myocardial depression were seen in patients anesthetized with halothane. Halothane, at least in a well-monitored environment, is safe for use in patients without severe ventricular dysfunction undergoing coronary-artery revascularization.

Anesthesia, General↗