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PubMed1984

[Blood pressure control with an inhalation anesthetic in acute intraoperative hypertension. Hemodynamic profile of halothane, enflurane and isoflurane in coronary surgery patients].

The haemodynamic effects of isoflurane, halothane and enflurane when used to control intraoperative hypertension were evaluated in 30 patients undergoing coronary artery bypass grafting. The patients were anaesthetized with flunitrazepam, fentanyl, pancuronium and N2O-O2. Control measurements were made after skin incision. When mean arterial pressure increased to 110 mmHg due to sternal spread or surgical manipulation of the aorta, halothane, enflurane or isoflurane were administered to return arterial pressure to control levels. Using a non-rebreathing system, inspired halothane concentrations of 1.0-1.5 vol.%, enflurane concentrations of 2.0-2.5 vol.% and isoflurane concentrations of 1.5-2.0 vol.% were necessary. Measurements were repeated during the hypertensive episodes and after treatment with halothane, enflurane or isoflurane while surgical stimulation continued. During the hypertensive episodes marked elevations in systemic vascular resistance were observed, four patients developed ischaemic ST-segment changes. Each of the three inhalational anaesthetics decreased mean arterial pressure to baseline values within 5 to 10 minutes. The fall in blood pressure caused by halothane was mainly due to a reduction in cardiac index, since the elevated systemic vascular resistance almost remained unaffected. Enflurane produced a similar fall in cardiac index, although left ventricular afterload was significantly reduced, suggesting that enflurane caused more impairment of cardiac performance than halothane. In contrast, the administration of isoflurane was associated with an increase of the cardiac index in the presence of marked systemic vasodilation and a slight decrease in left ventricular filling pressure. Halothane, enflurane and isoflurane reduced the rate-pressure product by a comparable degree and, when present, abnormalities in the ST-segments disappeared.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1984

Hemodynamic effects of amrinone in dogs anesthetized with halothane: comparison with isoproterenol and dobutamine.

Baseline hemodynamic variables were established during morphine - N2O-O2 anesthesia in dogs following which N2O was discontinued and halothane 2% (end-tidal) in O2 was administered. Halothane caused significant decreases of 58, 55, and 66 percent, respectively, in cardiac output, mean arterial pressure, and left ventricular dP/dt and significantly increased pulmonary vascular resistance (161%) when compared to measurements obtained under morphine - N2O-O2 anesthesia. During halothane anesthesia, amrinone, isoproterenol, and dobutamine were administered by continuous intravenous infusion in doses which restored cardiac output to pre-halothane values. Left ventricular dP/dt was increased and pulmonary resistance was decreased significantly by the three positive inotropic agents. Isoproterenol and amrinone significantly decreased systemic vascular resistance 48 and 71 percent, respectively below the value for halothane alone. Dobutamine significantly increased mean arterial pressure. Heart rate and left ventricular end-diastolic pressure were not altered by any treatment. Ventricular arrhythmias were associated with the infusion of all three agents. It is concluded that amrinone, isoproterenol, and dobutamine were capable of restoring cardiac output which had been decreased by halothane. However, isoproterenol and amrinone caused marked decreases in systemic vascular resistance which precluded an increase in arterial pressure above the value encountered with halothane alone.

Aminopyridines↗
PubMed1984

Isoflurane does not prevent hepatic injury produced by halothane in rats.

We speculated that the inhibitory effect of isoflurane on the metabolism of halothane might reduce hepatic injury produced by halothane. To test this hypothesis we pretreated male rats with phenobarbital and 24 hr later exposed them to one of three types of anesthesia. One group of rats was anesthetized with 0.6 MAC isoflurane in 21-25% oxygen for 20 min, followed by exposure to 0.3 MAC isoflurane and 0.3 MAC halothane either in 9% oxygen for 46 min (n = 5) or in 12% oxygen for 60 min (n = 11). A second group of rats received 0.3 MAC halothane in 9% oxygen for either 46 min (n = 12) or in 12% oxygen for 60 min (n = 10). The third group received 0.3 MAC isoflurane in 9% oxygen for either 46 min (n = 12) or for 120 min (n = 8). The rats were killed 24 hr after the exposures and liver slides prepared. Histologic examination revealed that rats treated with isoflurane plus halothane, or with halothane alone showed a significant hepatic injury (P less than 0.005) when compared with those treated with isoflurane. Thus isoflurane failed to protect the liver from halothane-induced injury.

Animals↗
PubMed1984

Halothane testing for malignant hyperthermia in swine: dose-response effects.

Purebred Pietrain malignant hyperthermia (MH)-susceptible pigs (n = 102) were subjected to halothane (0%, 1%, 2%, 3%, 4%, and 5%) in oxygen. The number of pigs in each group exhibiting muscle rigidity (MH(+) reaction) and the reaction times were recorded, as were the number of deaths resulting from MH. Mortality was not affected by the halothane concentration. However, halothane concentration did markedly affect the number of MH(+) reactions and the reaction times. False-negative reactions were apparent in the pigs at halothane concentrations less than 3%. Increasing the halothane concentration incrementally to 5% (from 0%) significantly (P less than 0.05) decreased reaction times between treatment groups. The reductions in reaction times which occurred in the pigs given the 3%, 4%, and 5% halothane concentrations (62.1, 56.2, and 50.05)--although significant (P less than 0.05)--would indicate that 3% halothane would generally be sufficient for MH testing.

Animals↗
PubMed1983

Comparison of isoflurane and halothane when used to control intraoperative hypertension in patients undergoing coronary artery bypass surgery.

The hemodynamic effects of isoflurane and halothane when used to control intraoperative hypertension were evaluated in 20 patients undergoing coronary artery bypass grafting. The patients were anesthetized with flunitrazepam, fentanyl, pancuronium, and N2O-O2. Control measurements were made after skin incision. When mean arterial pressure increased to 110 mm Hg due to sternal spread or surgical manipulation of the aorta, isoflurane or halothane were used to return arterial pressure to control levels. Using a non-rebreathing system, inspired isoflurane concentrations of 1.5-2.0 vol% or halothane concentrations of 1.0-1.5 vol% were necessary. Measurements were repeated during the hypertensive episode and after treatment with isoflurane or halothane while surgical stimulation continued. Both inhalation anesthetics decreased arterial pressure to baseline values within 5-10 min. The lowering of arterial pressure with halothane was not accompanied by significant decreases in the elevated systemic vascular resistance and pulmonary capillary wedge pressure. Cardiac index and stroke volume index decreased markedly when halothane was used (18% and 25%, respectively). In contrast, isoflurane significantly decreased systemic vascular resistance (42%). This reduction of left ventricular afterload was associated with an increase in cardiac index (22%) and a decrease in left ventricular filling pressure. Heart rate did not change significantly. These findings indicate that isoflurane is superior to halothane for controlling intraoperative hypertension during coronary artery bypass surgery.

Adult↗
PubMed1978

Potency of halothane-N20 in the horse.

The minimal alveolar concentration (MAC) of halothane which just prevented purposeful movement in response to electrical stimulation was determined in 11 young, healthy, unpremedicated horses breathing oxygen (O2) or nitrous oxide (N2O) and O2. Ventilation was controlled during these MAC studies. The arterial PO2 was always greater than 90 mm of Hg and the average PaCO2. range was 36 to 40 mm of Hg. The MAC for halothane in O2 was 0.93 vol %. Alveolar N2O concentrations of 25% and 50% reduced the halothane MAC about 12% and 25%, respectively. In 8 of these horses, the cardiovascular effects of halothane-50% N2O-balance O2 (H50N2O) were determined during spontaneous and controlled ventilation and were compared with previously reported results of halothane-O2 studies. Similar to halothane-O2 anesthesia, increasing dosages of H50N2O caused a decrease in cardiovascular function. With the exception of N2O-associated increase in cardiac output and left ventricular work at MAC 1.0 and 1.5, little difference was seen between the 2 forms of general anesthesia during controlled ventilation. However, when H50N20 was administered to spontaneously breathing horses, most indices of cardiovascular function were depressed less than with a similarly administered equipotent level (MAC 1.5) of halothane-O2 anesthesia.

Anesthesia, Inhalation↗
PubMed1983

Enflurane, halothane, and aminophylline--uptake and pharmacokinetics.

This study was designed to evaluate the effects of induction of enflurane or halothane anesthesia on the distribution and elimination of previously administered intravenous aminophylline, and to evaluate the effect of previously administered intravenous aminophylline on the uptake of enflurane or halothane. Fifty-four dogs were studied: 6 received no anesthetic, 24 received enflurane, and 24 halothane. The six animals receiving no anesthetic were given 10 mg/kg of aminophylline. In each of the two groups of 24 animals, six animals served as controls and received no aminophylline. Of the other 18 animals in each group, six received 10 mg/kg of aminophylline, six received 25 mg/kg of aminophylline, and six received 50 mg/kg of aminophylline intravenously before induction of enflurane or halothane anesthesia. The redistribution (alpha) phase of theophylline was similar when anesthesia was induced with either enflurane or halothane and slightly more rapid when no anesthetic was given following aminophylline administration. The elimination (beta) phase of theophylline in the presence of either anesthetic was not significantly different than when no anesthetic was administered. The uptake of enflurane or halothane was unaffected by prior administration of aminophylline. Differences in arrhythmogenicity between enflurane and halothane after aminophylline administration are not related to alterations in theophylline pharmacokinetics or anesthetic uptake.

Aminophylline↗
PubMed1980

Arrhythmogenic effects of aminophylline during halothane anesthesia in experimental animals.

Arrhythmogenic effects of aminophylline (theophylline ethylenediamine) during halothane anesthesia have been reported but have not been related to serum theophylline levels. This study was designed to determine the arrhythmogenicity of therapeutic and toxic serum theophylline levels during halothane anesthesia. The study consisted of three parts. In part 1 (induction) six dogs were anesthetized for 15 minutes with 1% halothane in air and then given intravenous aminophylline, 50 mg/kg. In part 2 (maintenance) eight dogs were anesthetized for 2 hours with 1% halothane and then given intravenous aminophylline, 10 mg/kg. In part 3, after four additional hours of steady-state 1% halothane anesthesia, additional intravenous aminophylline, 25 mg/kg, was given to these eight animals. Three of six dogs in part 1 had arrhythmias following aminophylline, with serum theophylline levels ranging from 48 to 66 mg/L. No dog in part 2 had arthythmias following the 10 mg/kg dose of aminophylline, with serum theophylline levels of 14 to 23 mg/L. Six of eight dogs in part 3 had arrhythmias shortly after aminophylline, 25 mg/kg, with serum theophylline levels of 36 to 72 mg/L. Aminophylline administration after prolonger 1% halothane anesthesia appears free from arrhythmogenic effects if serum theophylline levels remain near the therapeutic range (10 to 20 mg/L). Aminophylline administration resulting in high serum theophylline levels (above 36 mg/L) causes ventricular arrhythmias when aminophylline is given during induction or maintenance of 1% halothane anesthesia. Arrhythmias usually (89%) begin with 5 minutes of aminophylline administration, and these arrhythmias always resolve spontaneously within 2 minutes of onset.

Aminophylline↗
PubMed1980

Mechanical hyperventilation: effect on specialized atrioventricular conduction, supraventricular refractoriness, and experimental atrial arrhythmias in dogs anesthetized with pentobarbital or pentobarbital-halothane.

The effect of hypocapnia (PCO2ET 25 vs 40 torr) on specialized atrioventricular (AV) conduction, supraventricular refractory periods, and experimental atrial arrhythmias provoked by premature atrial stimulation (atrial echoes-echoes, repetitive atrial firing (RAF)) was assessed in dogs anesthetized with pentobarbital or pentobarbital-halothane (1.0% end-tidal). Catheter His bundle electrocardiography was used. Both hypocapnia and halothane prolonged AV nodal conduction, but the effect of halothane was more pronounced. Halothane prolonged the atrial functional (AtFRP), atrial effective (AtERP), and AV nodal functional refractory (AVFRP) periods. These effects of halothane were linked to an increased incidence of RAF but not to echoes. Hypocapnia prolonged the AVFRP (less than halothane), had no effect on the AtFRP and shortened the AtERP. These effects of hypocapnia were associated with an increased incidence of echoes, but not with RAF. Echoes and RAF are thought to be caused by reentry within the sinus node, atria, and AV node. The differing effects of halothane and hypocapnia on the incidence of these arrhythmias may be due to differning effects on supraventricular refractoriness.

Anesthesia↗
PubMed1981

Calcium transport by cardiac sarcoplasmic reticulum: modulation of halothane action by substrate concentration and pH.

The response of calcium transport to halothane by the cardiac sarcoplasmic reticulum (SR) was investigated to determine whether the SR is a site for anesthetic depression of the myocardium. It was observed that halothane could both stimulate (by 800%) and inhibit (by 500%) calcium transport. The varied effects are dependent on adenosine triphosphate (ATP) and calcium and hydrogen ion concentrations. At 2.25% halothane, the Km for ATP is decreased from 2.35 to 0.712 mM and Vmax is decreased from 292 to 149 nmoles/mg/2min. It was found that the steady-state level of calcium in the SR was decreased by 33% by halothane at pH 6.9, whereas halothane had no effect at pH 7.3. It was concluded that the SR is an unlikely site of halothane-induced myocardial depression in the normal heart when substrate concentrations and pH are maintained. In the ischemic heart in which the pH and substrate concentration have decreased, the interaction of halothane with the SR might contribute to a decrease in Ca2+ for contraction.

Adenosine Triphosphate↗
PubMed1982

Epinephrine-induced arrhythmias during halothane anesthesia with the addition of nitrous oxide, nitrogen, or helium in dogs.

The arrhythmogenicity of epinephrine was examined in 34 male mongrel dogs awake and during 1.1 MAC steady state halothane-O2 anesthesia with the addition of 50% N2O, nitrogen, or helium. All anesthetized dogs required more epinephrine than did awake dogs to produce ventricular extrasystoles. Dogs given halothane-N2O were more sensitive to the epinephrine infusion than those given halothane-nitrogen or halothane-helium. The dogs given halothane-N2O also showed a small, but statistically significant difference from dogs given halothane-O2. These results suggest that the addition of N2O to halothane increases the cardiac arrhythmic potential of epinephrine in the dog.

Animals↗
PubMed1980

[The metabolism of halothane under the influence of thiopental, methohexital, etomidate, enflurane and disulfiram under clinical conditions (author's transl)].

The biotransformation of halothane is supposed to be the cause of the rare "halothane-hepatitis". Therefore an inhibition of the metabolism of Halothane is of some interest. We used bromide as a metabolite of Halothane and investigated the bromide level of the serum of patients after halothane anaesthesia by means of x-ray fluorescence spectrometry. The induction of anaesthesia with Thiopental, Methohexital and Etomidate had no influence on the bromide level. Likewise the influence of Enflurane on the metabolism of Halothane was not significant. An effective inhibitor in man is Disulfiram. The authors assume, that further information about the toxicity of Halothane metabolites can be gained through further studies of drugs like Disulfiram.

Adolescent↗
PubMed1994

[Effects of sevoflurane or halothane on contractile responses of isolated canine basilar artery].

Although volatile anesthetic is known as a cerebral vasodilator, its mechanism is not clear. The purpose of this study was to investigate effects of sevoflurane or halothane on contractions induced by high K+ and serotonin in the isolated canine basilar artery. Cylindrical segments of canine basilar artery were placed in Krebs solution oxygenated with 95% O2 and 5% CO2 at 37 degrees C. They were then constricted with cumulative administration of 10 to 60 mM KCl, or with 10(-9) to 10(-6) M serotonin and exposed to either sevoflurane or halothane at concentration of 1.0 and 2.0 MAC. Halothane and sevoflurane at concentration of 1.0 and 2.0 MAC decreased contractile responses evoked by KCl to a similar degree. The attenuation by either of the two anesthetics at concentration of 2.0 MAC were equivalent to the inhibitions by diltiazem 2 x 10(-7) M. Contractile responses to serotonin above 3 x 10(-7) M were depressed by halothane 1.0 MAC, but not by sevoflurane 1.0 MAC. Sevoflurane and halothane at concentration of 2.0 MAC decreased contractile responses evoked by serotonin at concentrations above 3 x 10(-8) M and 10(-8) M. Removal of the endothelium did not alter the response of the basilar artery contracted by serotonin to either anesthetic. These findings suggest that sevoflurane and halothane depress the voltage-dependent Ca2+ channels due to decreases of contractile responses to high K+. Our results also demonstrate that sevoflurane is a less potent vasodilator of the basilar artery contracted by serotonin than halothane.

Animals↗
PubMed1993

Effect of halothane exposure on motor skills & memory in anaesthetists.

In a prospective study involving 24 anaesthesia residents, each resident was assessed three times i.e., first as control group, not exposed to anaesthesia at all; the second group in which the resident was exposed to anaesthesia while using controlled respiration with closed circuit without halothane (non-halothane group) and the third group in which they were exposed to anaesthesia using spontaneous respiration with semiclosed circuit using halothane (halothane group). After each exposure of 3-4 h duration in each group, the resident was subjected to specific psychological tests to assess motor skills and memory. In the non-halothane group, a depression of motor skills by 5.51 per cent and of memory by 17.14 per cent was observed. In the halothane group, the reduction of motor skills was up to 27 per cent and of memory by 45 per cent as compared to the control values. It is concluded that 3-4 h exposure to halothane (1.5-4%) obtunds the motor skills and memory in anaesthetists.

Adult↗
PubMedDate not supplied

A comparison of the effects of halothane and isoflurane in combination with nitrous oxide on lower oesophageal sphincter pressure and barrier pressure in anaesthetised dogs.

The effects of surgery, and of halothane and isoflurane, on oesophageal pressures were examined in 30 dogs. The dogs were premedicated with a combination of acepromazine maleate (0.1 mg/kg) and pethidine hydrochloride (1 mg/kg), and anaesthesia was induced with thiopentone (10 mg/kg). Ten of the dogs underwent abdominal surgery with halothane, 10 underwent abdominal surgery with isoflurane and 10 underwent non-abdominal surgery with halothane. Gastric pressure, lower oesophageal sphincter pressure and oesophageal barrier pressures were measured at five to 10 minutes after induction, five to 10 minutes after the initial surgical incision, during the abdominal surgery and while the skin was being sutured. There were no significant differences in lower oesophageal sphincter pressure between the groups of dogs but the pressures were greater in all the dogs during the surgical manipulation than shortly after induction or while the skin was being sutured. During abdominal surgery with halothane the barrier pressure was significantly higher (P < 0.05) than during non-abdominal surgery with halothane. The barrier pressure was lower (P < 0.001) during skin suturing after abdominal surgery with isoflurane than after abdominal or non-abdominal surgery with halothane. The lower oesophageal sphincter appears to be more sensitive to isoflurane than halothane.

Abdomen↗
PubMed1998

Quantitative autoradiography of halothane binding in rat brain.

14C-halothane direct photoaffinity labeling was used to characterize the distribution of halothane binding in rat brain to test the hypothesis that anesthetics bind preferentially to a specific, heterogeneously distributed, receptor or channel. Slide-mounted sagittal rat brain sections were placed in gas-tight quartz cuvettes with 100 microM 14C-halothane in phosphate buffered saline with 0 to 7.5 mM unlabeled halothane, or unlabeled chloroform and isoflurane at 10 times the clinical EC50, and then exposed to UV light for 60 to 100 sec. Autoradiograms of nine brain regions (cortex, corpus callosum, hippocampal molecular and pyramidal layers, dentate molecular and granule cell layers, and cerebellar molecular, granular and white matter layers) were prepared and quantitated using Image 1.44. Total label incorporation was widespread, but exhibited subtle heterogeneity. There was significantly more total labeling in regions of high synaptic density than in regions containing primarily cell bodies or white matter. Most labeling (approximately 80%) was displaced by unlabeled halothane and can therefore be considered specific. Significantly more specific labeling was found in regions of high synaptic density. Isoflurane did not inhibit halothane photolabeling significantly, but chloroform inhibited it by approximately 50%. In conclusion, halothane photolabeling distribution in the mammalian brain is widespread, saturable and selective, but does not mimic the distribution of any individual receptor or channel. Brain regions with high synaptic density displayed the greatest degree of specific binding, consistent with transmission being an important functional target of volatile anesthetics. These results suggest a remarkably widespread individual target, or more likely, similar binding sites in multiple targets, and are consistent with the notion that anesthesia is the result of action at multiple sites.

Anesthetics, Inhalation↗
PubMed1998

Halothane-induced acute liver failure: continuing occurrence and use of liver transplantation.

BACKGROUND/AIMS: This study was aimed at determining if the frequency and pattern of acute liver failure (ALF) following halothane anaesthesia had decreased during the last 11 years in comparison with a previous series of 48 patients referred between 1965 and 1984 and whether clinical outcome had been altered by the introduction of liver transplantation. METHODS: Between January 1985 and December 1995, all patients with halothane-induced ALF admitted to the Liver Failure Unit at King's College Hospital were identified. Four other European liver transplant centres with a known interest in acute liver failure also provided data. RESULTS: Of the 18 patients admitted, the clinical data were complete in 15. Ten of these patients had at least one previous halothane anaesthesia with documented clinical complications following the earlier exposure in six. Four patients had been re-exposed to halothane within 1 month of the penultimate halothane anaesthesia. Of the 15 patients four survived with medical management alone and 11 patients fulfilled transplant criteria. Four of the latter group were not listed because of rapidly deteriorating medical state and died, and of the seven patients who were listed, three died without a liver becoming available and four were transplanted, one of whom survived. No patient who had grade 4 encephalopathy and a prothrombin time > 50 s survived without a transplant. The survey of the other European liver centres recorded a total of 19 patients with halothane-induced ALF including three cases reported in the literature. Of those, 13 patients had been transplanted with nine survivors. CONCLUSION: Cases of halothane-induced acute liver failure still occur, albeit at a lower frequency than previously, and the Committee on Safety of Medicines guidelines are not being followed. The results of transplantation in these patients are encouraging.

Adult↗
PubMed1998

Anesthetic potency and cardiopulmonary effects of sevoflurane in goats: comparison with isoflurane and halothane.

The anesthetic potency and cardiopulmonary effects of sevoflurane were compared with those of isoflurane and halothane in goats. The (mean +/- SD) minimal alveolar concentration (MAC) was 0.96 +/- 0.12% for halothane, 1.29 +/- 0.11% for isoflurane, and 2.33 +/- 0.15% for sevoflurane. Cardiopulmonary effects of sevoflurane, halothane and isoflurane were examined at end-tidal concentrations equivalent to 1, 1.5 and 2 MAC during either spontaneous or controlled ventilation (SV or CV). During SV, there were no significant differences in respiration rate, tidal volume and minute ventilation between anesthetics. Dose-dependent decreases in both tidal volume and minute ventilation induced by halothane were greater than those by either sevoflurane or isoflurane. Hypercapnia and acidosis induced by sevoflurane were not significantly different from those by either isoflurane or halothane at 1 and 1.5 MAC, but were less than those by halothane at 2 MAC. There was no significant difference in heart rate between anesthetics during SV and CV. During SV, all anesthetics induced dose-dependent decreases in arterial pressure, rate pressure product, systemic vascular resistance, left ventricular minute work index and left ventricular stroke work index. Systemic vascular resistance with isoflurane at 2 MAC was lower than that with sevoflurane. During CV, sevoflurane induced dose-dependent circulatory depression (decreases in arterial pressure, cardiac index, rate pressure product, systemic vascular resistance, left ventricular minute work index and right ventricular minute work index), similar to isoflurane. Halothane did not significantly alter systemic vascular resistance from 1 to 2 MAC.

Anesthetics, Inhalation↗