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PubMed1982

Teaching the uptake and distribution of halothane. A computer simulation program.

A computer aided learning program for teaching the kinetics of uptake and distribution of the inhalational anaesthetic halothane is described. The program is based on a seven-compartment model which simulates the action of halothane on ventilation and on the cardiovascular system. The program is available to the student in four forms: one with no changes in circulation or respiration, one with the cardiovascular effects of halothane included, one with respiratory effects only, and one with both of these effects combined. The student can study the importance of the influence of halothane on respiration and blood circulation by comparing results from simulations on different models. The simulation is presented as graphs which are continuously displayed on an alphanumeric visual display terminal. Interaction with the program is possible at all times to change the simulation speed, the variables being graphed, the inspired halothane fraction, and the fresh gas flow.

Anesthesia, Inhalation↗
PubMed1983

Postoperative jaundice in children. The influence of halothane.

At the Hospital for Sick Children, Great Ormond Street, during the 23-year period 1957 to 1979, 165400 anaesthetics were administered. Almost all of the patients anaesthetised during this time would have been exposed to halothane. Seventy-four patients became jaundiced for the first time in the post-operative period. Halothane-associated hepatitis was excluded as the cause of the postoperative jaundice in all but two of the 74 patients. In these two patients in whom the diagnosis of halothane-associated hepatitis was possible the hepatitic illness was mild and both patients made an uneventful recovery. In this survey the risk of a patient becoming jaundiced due to halothane associated hepatitis was greater than 1 in 82000. It would seem that in children halothane can be used whenever it is warranted and can be used repeatedly.

Adolescent↗
PubMed1996

A comparison of the induction characteristics of sevoflurane and halothane in children.

The induction characteristics of sevoflurane and halothane were compared in 81 children aged 6 months to 6 years. The mean time taken to achieve loss of eyelash reflex was significantly shorter with sevoflurane than with halothane (sevoflurane, mean time (SD) 1 min 41 s (35 s), halothane, mean time (SD) 2 min 17 s (43 s), t = 4.11, p = < 0.01). The mean time taken to complete induction (to achieve steady spontaneous ventilation and small pupils with central gaze) was also shorter in children induced with sevoflurane (sevoflurane, mean time (SD) 3 min 58 s (1 min 8 s), halothane, mean time (SD) 4 min 50 s, (1 min 27 s), t = 2.29, p = 0.027). Effects on heart rate, blood pressure and oxygen saturation during induction were similar for both agents. There were no major complications during induction with either halothane or sevoflurane.

Anesthesia, Inhalation↗
PubMed1996

Anaesthesia and the QT interval in humans. The effects of isoflurane and halothane.

Prolongation of the QT interval may cause potentially hazardous arrhythmias. The effects on the QT interval (QTc, corrected for heart rate) of isoflurane and halothane followed by vecuronium have been investigated during induction of anaesthesia in 51 patients. All patients were ASA 1 or 2, without cardiovascular problems or electrolyte abnormalities and were not receiving medication. Midazolam 0.08 mg.kg-1 was administered intramuscularly for premedication. Anaesthesia was induced with either isoflurane (n = 26) or halothane (n = 25), and the inspired concentration increased to reach an end-tidal concentration of 2.5% to 3%. Recordings of ECG, heart rate, systolic and diastolic arterial pressure were obtained at the following times: prior to induction of anaesthesia; 1 min and 3 min after a stable end-tidal concentration had been reached; 1 min and 3 min following vecuronium administration, at the time of tracheal intubation and 1 min and 3 min later. Halothane significantly shortened QTc (p < 0.05 to p < 0.001), in contrast to isoflurane which prolonged it (p < 0.01). The heart rate decreased (p < 0.01 to p < 0.001) after induction of anaesthesia with halothane and returned to pre-induction values after tracheal intubation. In contrast, heart rate increased after induction with isoflurane and increased further after laryngoscopy and tracheal intubation (p < 0.001). In the isoflurane group, ST depression was noticed in seven patients and nodal rhythm in two, while in the halothane group seven patients developed nodal rhythm and, in two patients, ventricular ectopics were recorded. There were no sequelae. In both groups, systolic and diastolic arterial pressure decreased after induction of anaesthesia (p < 0.01 to p < 0.001), increasing again after intubation.

Adolescent↗
PubMed1976

Restoration of oxygen uptake and blood flow in the rat cerebral cortex after halothane anaesthesia.

Halothane decreases both the cerebral blood flow (CBF) and the cerebral metabolic rate for oxygen (CMRO2) when given in anaesthetic doses. A recent report (GJEDDE & HINDFELT 1975) suggests that when halothane is administered to rats for 1 hour, CBF and CMRO2 are depressed by about 30 and 40%, respectively, for as long as 4 hours after discontinuation of the halothane anaesthesia. In the present study rats were anaesthetized with 1% halothane for 1 hour, and CBF and CMRO2 were measured at the end of a 30 min recovery period, during which 70% N2O was administered. Comparison with animals maintained on 70% N2O throughout the entire 90 min period showed that previous halothane anaesthesia had no effects on CBF or CMRO2.

Anesthesia, General↗
PubMed1978

The hemodynamic effect of halothane in the normovolemic dog.

With the aid of radioactive microspheres (labeled with 169Yb, 85Sr and 141Ce, respectively), the effect of halothane anesthesia on circulation was studied for 30 min and (group A) for 120 min of halothane anesthesia in thiopental-sedated dogs. Measurements were also carried out on recovery from halothane anesthesia. Besides such well-known general circulatory changes as reduction in cardiac output, pulse rate, left ventricular work, arterial mean blood pressure and left atrial mean blood pressure, in both groups there was also a reduced coronary blood flow. The flow to the lungs, kidneys and the brain was well preserved, despite the reduction in both the cardiac output and arterial mean blood pressure. The flow to the liver, however, did not change during short halothane anesthesia; but during long anesthesia there was a marked reduction, due mainly to a decrease in the flow to the preportal area. On recovery from halothane anesthesia, the changes had mostly returned to the preanesthetic values.

Anesthesia, Inhalation↗
PubMed1979

The potentiation of halothane anaesthesia by clonidine.

The antihypertensive agent, clonidine, has a marked sedative effect. We studied whether clonidine also deepens halothane anaesthesia. Eight rabbits were anaesthetized with and without clonidine premedication in a cross-over study. Clonidine premedication (50 microgram/kg subcutaneously) was administered three times daily for 3 days. Tolerance to pain during halothane anaesthesia was tested by compressing the ear with a vessel clamp. Halothane concentrations were determined by gas chromatography. The rabbits premedicated with clonidine tolerated painful stimuli without reactions at lower halothane concentrations in arterial blood and inspired air than unpremedicated rabbits. MAC calculated from blood concentrations was 1.29% for unpremedicated and 1.09% for clonidine-premedicated rabbits. The results suggest that clonidine diminishes the anaesthetic requirement in halothane anaesthesia.

Adjuvants, Anesthesia↗
PubMed1980

Temperature-dependent nerve-blocking action of lidocaine and halothane.

The effect of lidocaine and halothane on the compound action potential of rat sciatic nerves was studied under hypo-hyperthermic conditions. In drug-free desheathed nerves, a total but reversible cold block occurred at 10-11 degrees C, and an irreversible heat block at 46 degrees C. Cooling potentiated the dose-dependent blocking action of lidocaine (decreased amplitude, and increased duration and latency of the compound action potential). Total block of conduction occurred at 17 degrees C with 100 microM lidocaine, at 20 degrees C with 200 microM lidocaine and at 24 degrees microM with 400 microM lidocaine. In nerves equilibrated in 200 microM lidocaine solution, the lidocaine concentrations in the nerves decreased as the temperature decreased; at 20 degrees C, the lidocaine concentration was about half of that at 37 degrees C. The nerve-blocking effect of lidocaine was also potentiated by increasing the temperature above 37 degrees C. At 30 degrees C and 20 degrees C, 1 vol. % halothane caused a slight time-dependent inhibition of the compound action potential. When the nerves were exposed to 2.5 vol. % halothane, the decrease in amplitude and increase in duration and latency were potentiated by hypothermia and were also time dependent. Interaction of halothane and temperature of 40 degrees C was not significant. Although thermodynamic principles suggest similarities between high pressure and cooling in reversing anaesthesia, cooling was found to potentiate the anaesthetic effect of lidocaine and halothane in this study. Temperature may thus be an interesting physical variable in studying nerve-blocking mechanisms.

Action Potentials↗
PubMed1981

Effects of incremental halothane levels on the reflex responses to carotid hypotension in the dog.

Arterial baroreceptor function was assessed in trained, chronically instrumented dogs by measuring the systemic haemodynamic responses to brachiocephalic artery occlusion (BCO). BCO was carried out in awake dogs and repeated at end-tidal halothane levels of 0.75 +/- 0.01% (H1), 0.94 +/- 0.02% (H2) and 1.13 +/- 0.02% (H3). Before BCO, at H1 only the increased heart rate and decreased stroke volume were significantly different from awake controls (P less than 0.01). Mean atrial pressure and cardiac output at H2 and H3 were significantly lower than in the awake controls (P less than 0.05). The pressor response to BCO fell progressively with increasing halothane levels, the decrease being significant at the H2 and H3 levels (P less than 0.001). There was a good linear correlation between the pressor response to BCO as a percentage of the response in awake animals, and the end-tidal halothane levels (r = -0.816, P less than 0.001). This indicated a sensitive dose-dependent modification of the haemodynamic response to BCO by halothane. However, halothane levels existed between about 0.7-0.8%, at which levels the average pressor response to BCO was not significantly different from awake values.

Anesthesia, Inhalation↗
PubMed1982

Effect of mannitol and furosemide on urinary fluoride excretion of surgical patients anaesthetized with enflurane or halothane.

Urinary excretion of fluoride after enflurane anaesthesia has been found to correlate with urinary pH, while the correlation with urinary volume has remained unsettled. We therefore studied the effect of moderate doses of mannitol and furosemide on serum fluoride levels and urinary excretion of fluoride in surgical patients after controlled doses of enflurane (6+6+6 patients) or halothane (5+5+5 patients). The highest serum fluoride level was 31 mumol/1 in an enflurane patient (enflurane dose 1.26 end-tidal vol % x h) and 8 mumol/1 in a halothane patient (halothane dose 0.59 end-tidal vol. % x h). Mannitol caused th greatest mean excretion of fluoride (not significant (n.s)) in the enflurane patients without any marked rise in urinary pH or volume. Furosemide increased urinary output markedly but did not enhance urinary fluoride excretion or raise urinary pH. Compared with the control groups of both inhalation anaesthetic patients, the diuretics appeared to have no effect on the serum fluoride levels. In the enflurane patients there was a positive correlation between the change in fluoride clearance and the change in urinary pH, but no with the change in urinary volume during the first postoperative hours. On the other hand, in the halothane patients there was a positive correlation between the change in fluoride clearance and the change in urinary volume. A possible "fluoro-uretic" action of mannitol was also seen in the halothane patients, as in the later postoperative period fluoride excretion was greatest when mannitol had been given.

Adult↗
PubMed1983

Circulatory effects of renin-angiotensin system antagonists during halothane anaesthesia in hypertensive rats.

The circulatory effects of captopril, an angiotensin I-converting enzyme inhibitor, and saralasin, a competitive angiotensin II antagonist, were studied during halothane anaesthesia in spontaneously hypertensive (SH) rats. Captopril decreased blood pressure significantly in unanaesthetized rats. Pretreatment with indomethacin, a prostaglandin synthesis inhibitor, did not modify the antihypertensive action of captopril. During 1 MAC halothane anaesthesia, the mean arterial pressure (MAP) in unmedicated SH control rats was maintained at a relatively high level (16.2 +/- 0.7 kPa, mean +/- s.e. mean), while in captopril-treated rats MAP decreased to 8.8 +/- 1.1 kPa. Indomethacin somewhat inhibited MAP decrease in the captopril-medicated group. Saralasin infusion in halothane-anaesthetized rats decreased MAP in the same way as captopril alone. The tolerance to haemorrhagic shock was markedly impaired in rats receiving captopril or saralasin, compared to untreated controls. During halothane anaesthesia, the plasma renin activities in the captopril, captopril + indomethacin, and saralasin groups were significantly higher than in untreated animals. Plasma kininogen was unaffected by any of the medications. The results suggest that the renin-angiotensin system is important in maintaining blood pressure in halothane anaesthesia, and that the tolerance to haemorrhagic shock is particularly impaired by drugs inhibiting the renin-angiotensin system.

Angiotensin II↗
PubMed1985

Comparative maternal and neonatal effects of halothane and enflurane for cesarean section.

The effects of placental transfer of enflurane and halothane were studied in 81 women undergoing cesarean sections. All patients had rapid sequence induction using thiopental, succinylcholine, and endotracheal intubation. They were then randomly assigned to one of five groups: Group I (n = 16) received N2O and oxygen, Group II (n = 16) N2O, oxygen, and 0.25% halothane, Group III (n = 18) N2O, oxygen, and 0.5% halothane, Group IV (n = 18) N2O, oxygen, and 0.5% enflurane, Group V (n = 13) N2O, oxygen, and 1% enflurane. At delivery, blood was drawn from the maternal artery, umbilical vein and artery for measurement of the halogenated agents using gas chromatography. The neonates were evaluated by Apgar scores, umbilical artery and vein acid base status and the Early Neonatal Neurobehavioral Scores (ENNS) at 2 and 24 h of age. Blood loss and the incidence of maternal awareness were also determined. The umbilical vein to maternal vein ratio was approximately 0.5 and 0.6 for enflurane and halothane, respectively. The umbilical artery to umbilical vein ratio was 0.5 with both agents; higher inspired anesthetic concentrations produced higher blood levels. All neonates had Apgar scores of 8 or more at 5 min with the exception of one neonate in the N2O group. Maternal and neonatal acid base status, blood loss, and ENNS were not affected by the addition of the halogenated agents. Of the patients who had N2O alone, 12% had awareness versus none in the other groups. These data demonstrate that low dose halothane or enflurane decreases the incidence of maternal awareness and does not adversely affect the neonate.

Adult↗
PubMed1987

Halothane, enflurane and isoflurane anaesthesia for adenoidectomy in children, using two different premedications.

In 48 children subjected to adenoidectomy, comparisons of airway problems, heart rates, cardiac arrhythmias, ventilation and stress hormone reactions were studied during halothane, enflurane and isoflurane anaesthesia. Sixteen children were anaesthetized with either of the three agents and eight patients in each group received diazepam 0.25 mg kg-1 and atropine 0.015 mg kg-1 rectally (DA) as premedication and the remainder diazepam 0.5 mg kg-1, morphine 0.15 mg kg-1 and scopolamine 0.01 mg kg-1 (DMS) rectally. All children were intubated and breathing spontaneously. Equianaesthetic inspired concentrations of halothane, enflurane and isoflurane were used. Airway problems were of the same magnitude during halothane and isoflurane anaesthesia but were less frequent with both agents compared with enflurane anaesthesia. DMS reduced the number of airway reactions in all groups. Respiratory rates were uninfluenced by anaesthesia, intubation and surgery during enflurane anaesthesia. Cardiac arrhythmias were less frequent with enflurane and isoflurane than with halothane. Plasma ACTH and cortisol were similar with all three agents. During induction of anaesthesia in the DA-premedicated halothane group, however, plasma catecholamines were higher than in the group which received DMS, in contrast to the findings during enflurane and isoflurane anaesthesia. The DMS premedication decreased the response of plasma ACTH, cortisol and plasma catecholamines to surgery.

Adenoidectomy↗
PubMed1988

Effects of halothane on membrane potentials and membrane ionic currents in single bullfrog atrial cells.

Halothane exerts negative inotropic and negative chronotropic actions on the isolated heart in experimental animals. In order to assess directly the actions of halothane in myocardium, we studied the effects of halothane on membrane potentials and transmembrane ionic currents in single isolated frog atrial cells obtained by the enzymatic dissociation method. The results show: (a) that the action potential is prolonged and its plateau phase and overshoot are depressed, but the resting potential remains unchanged; (b) that there is a significant inhibition of a time- and voltage-dependent outward K+ current and a slow inward Ca2+ current, with a slight decrease of a fast inward Na+ current following halothane (1.0-4.0%) application; and that halothane has no effect on another K+ current, time-independent current.

Animals↗
PubMed1989

Halothane-induced variability in the neuromuscular transmission of patients with myasthenia gravis.

The purpose of the present clinical study was to explore the skeletal muscle mechano (MMG)- and electromyographic (EMG) responses during halothane/oxygen/air anaesthesia in patients with myasthenia gravis (MG) compared with patients with normal neuromuscular transmission. The majority of MG-patients had a significant decremental response of the evoked muscle action potentials to a train-of-four (TOF) stimulation during halothane exposure (mean decrease of train-of-four ratio was 33% during the highest mean halothane concentration of 1.9 MAC). An excellent correlation was found between MMG- and EMG-measurements (r2 = 0.878, P less than 0.001). However, marked individual variations in the neuromuscular response to halothane were seen. Neither preoperative muscle fatigability nor acetylcholine receptor antibodies predicted the decremental muscle responses produced by halothane among MG-patients. The increased presence of HLA-B8 among myasthenics with halothane-suppressed muscle responses after TOF stimulation could be demonstrated (P less than 0.01).

Adolescent↗
PubMed1989

Displacement of warfarin from human serum proteins by halothane anaesthesia.

The in vitro effects of the halothane metabolite, trifluoroacetic acid, on the binding of warfarin to human serum proteins have been investigated. An increase in the percentage of free warfarin following incubation with different concentrations of trifluoroacetic acid (1 and 4 mmol/l) was observed. In addition, protein binding of warfarin was studied in serum from patients undergoing halothane anaesthesia (1-2.5%; 2.5 h). After 24 h from the end of the halothane anaesthesia, an increase in the percentage of free warfarin was also detected (0.92 +/- 0.06% at 24 h vs 0.60 +/- 0.02% before halothane administration; P less than 0.005). We conclude that halothane anaesthesia may temporarily potentiate the pharmacological effect of warfarin in the postoperative period following anaesthetic procedures.

Adult↗
PubMed1990

Effects of halothane on the efflux of [3H]D-aspartate from rat brain slices.

The in vitro effects of halothane on the potassium-stimulation-induced efflux of [3H]D-aspartate in rat cerebral cortex slices were studied. The slices were initially incubated with Krebs-Ringer's solution containing [3H]D-aspartate, a putative excitatory transmitter. The slices were then stimulated with high concentrations of K+ in the presence and absence of halothane, and the efflux was measured using a scintillation counter. Halothane, 1% and 2%, had little effect on the potassium-stimulation-induced efflux, but that of 4 and 8% increased the efflux significantly. The spontaneous efflux was unaffected by all concentrations of halothane studied. The control study of pentobarbital, in the concentration of 0.05 to 1.00 mmol/l, reduced the efflux in a dose-related manner. These findings indicate that the release of an excitatory transmitter, aspartate, may not be involved in the mechanism of halothane anaesthesia.

Animals↗
PubMed1995

Oxygen tension-associated changes on secondary immune response in halothane or isoflurane anesthetized mice.

The impact that reexposure to anesthetics delivered in 100% oxygen or in synthetic air (21% oxygen/79% nitrogen) has on the secondary humoral immune response to sheep red blood cells was studied. Mice were immunized twice with a 15-day interval and anesthetized immediately after each antigenic challenge with 1.5% halothane or 1.5% isoflurane for 40 min. Halothane in oxygen resulted in increased numbers of IgG-secreting cells (IgG-SC), while halothane in air depressed the response when compared to control mice. In contrast, isoflurane vaporized in oxygen did not affect IgG-SC numbers, while isoflurane given in air lowered the response. Furthermore, neither 100% oxygen, nor the stress of being in an anesthesia chamber breathing synthetic air for 40 min had any immunological effect in non-anesthetized mice. The inspired oxygen concentration during halothane or isoflurane anesthesia has an effect on the secondary immune response. The effect is different between halothane and isoflurane, possibly due to differences in the extent of their metabolic and pharmacodynamic properties.

Anesthetics, Inhalation↗