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PubMed1999

Halothane enhances exocytosis of [3H]-acetylcholine without increasing calcium influx in rat brain cortical slices.

1. The effect of halothane on the release of [3H]-acetylcholine ([3H]-ACh) in rat brain cortical slices was investigated. 2. Halothane (0.018 mM) did not significantly affect the basal and the electrical field stimulation induced release of [3H]-ACh. However, halothane (0.063 mM) significantly increased the basal release of [3H]-ACh and this effect was additive with the electrical field stimulation induced release of [3H]-ACh. 3. The release of [3H]-ACh induced by 0.063 mM halothane was independent of the extracellular sodium and calcium ion concentration and was decreased by tetracaine, an inhibitor of Ca(2+)-release from intracellular stores or dantrolene, an inhibitor of Ca(2+)-release from ryanodine-sensitive stores 4. Using 2-(4-phenylpiperidino)-cyclohexanol (vesamicol), a drug that blocks the storage of ACh in synaptic vesicles, we investigated whether exocytosis of this neurotransmitter is involved in the effect of halothane. Vesamicol significantly decreased the release of [3H]-ACh evoked by halothane. 5. It is suggested that halothane may cause a Ca2+ release from intracellular stores that increases [3H]-ACh exocytosis in rat brain cortical slices.

Acetylcholine↗
PubMed2000

Effects of halothane on the membrane potential in skeletal muscle of the frog.

Halothane has many effects on the resting membrane potential (V(m)) of excitable cells and exerts numerous effects on skeletal muscle one of which is the enhancement of Ca(2+) release by the sarcoplasmic reticulum (SR) resulting in a sustained contracture. The aim of this study was to analyse the effects of clinical doses of halothane on V(m), recorded using intracellular microelectrodes on cleaned and non stimulated sartorius muscle which was freshly isolated from the leg of the frog Rana esculenta. We assessed the mechanism of effects of superfused halothane on V(m) by the administration of selective antagonists of membrane bound Na(+), K(+) and Cl(-) channels and by inhibition of SR Ca(2+) release. Halothane (3%) induced an early and transient depolarization (4.5 mV within 7 min) and a delayed and sustained hyperpolarization (about 11 mV within 15 min) of V(m). The halothane-induced transient depolarization was sensitive to ryanodine (10 microM) and to 4-acetamido-4'-isothiocyanatostilbene 2,2' disulphonic acid (SITS, 1 mM). The hyperpolarization of V(m) induced by halothane (0.1 - 3%) was dose-dependent and reversible. It was insensitive to SITS (1 mM), tetrodotoxin (0.6 microM), and tetraethylammonium (10 mM) but was blocked and/or prevented by ryanodine (10 microM), charybdotoxin (CTX, 1 microM), and glibenclamide (10 nM). Our observations revealed that the effects of halothane on V(m) may be related to the increase in intracellular Ca(2+) concentration produced by the ryanodine-sensitive Ca(2+) release from the SR induced by the anaesthetic. The depolarization may be attributed to the activation of Ca(2+)-dependent Cl(-) (blocked by SITS) channels and the hyperpolarization to the activation of large conductance Ca(2+)-dependent K(+) channels, blocked by CTX, and to the opening of ATP-sensitive K(+) channels, inhibited by glibenclamide.

Anesthetics, Inhalation↗
PubMed1977

Rates of glucose utilization and glucogenesis in rats in the basal state induced by halothane anaesthesia.

1. Rates and rate coefficients of glucose utilization and replacement were determined with [5-3H]- and [U-14C]-glucose in rats starved for 24h, either conscious or under halothane anaesthesia, in a thermoneutral environment. Plasma insulin concentrations were also measured. 2. Halothane anaesthesia decreased the turnover rate by 20%, which was similar to previously reported decreases in metabolic rates caused by natural sleep. 3. Fractional recycling of glucose carbon was little affected by halothane. 4. Comparison of values in one rat with those in another, among both conscious rats and those under halothane anaesthesia, showed that rate coefficients were inversely correlated with plasma glucose concentrations. 5. These findings indicated that halothane, in the concentration used (1.25%, v/v), had little specific effect on glucose metabolism. 6. Although equilibrium plasma glucose concentrations in different rats under halothane were widely different (4-8 mmol/l) the rates of utilization were very similar (2.5-3.1 micronmol/min per 100 g), indicating that these rates were determined by the production of glucose from gluconeogenic precursors released by basal metabolism, the rate of which is necessarily similar in different rats. 7. Among rats under halothane anaesthesia plasma insulin concentrations were negatively correlated with rate coefficients, showing that the differences between rate coefficients were mostly accounted for by differences between rats in tissue sensitivities to insulin. Thus in each 24h-starved rat, sleeping or resting, the main regulators of the plasma glucose concentrations were the rate of supply of gluconeogenic substrates from energy metabolism and the intrinsic sensitivity of the tissues to insulin. 8. We found that a commonly used deionization method of purifying glucose for determination of its specific radioactivity was inadequate.

Anesthesia, Inhalation↗
PubMed1977

Glucose turnover in the post-absorptive rat and the effects of halothane anaesthesia.

1. Rates and rate coefficients of glucose utilization and replacement in post-absorptive rats, either conscious or under halothane anaesthesia, were determined in a thermoneutral environment by using [5-3H]- and [U-14C]glucose. Label was not injected into rats under halothane until about 0.5h after anaesthesia was initiated. 2. Comparison with the results for 24h-starved rats in the preceding paper [Heath et al. (1977) Biochem. J. 162, 643-651] showed that insulin concentrations were considerably higher but rate coefficients for glucose utilization were little altered in post-absorptive rats. Sensitivity to insulin was thus considerably increased by a 24h period of starvation in the rat. 3. Fractional recycling of glucose carbon in post-absorptive rats was under one-half of that in starved rats, reflecting the larger contribution of liver glycogenolysis to glucose production in the former. 4. In post-absorptive rats halothane decreased the mean rate of glucose utilization by about 17%. This decrease was associated with an increase in mean plasma insulin concentration, showing that halothane decreased sensitivity to insulin. 5. Recycling was slightly increased by halothane, indicating that the contribution of liver glycogen to the total glucogenic rate was decreased, probably because liver glycogen concentration were about 40% lower throughout the rate determinations in halothane. 6. Comparison of our results with earlier work shows that during and shortly after induction of halothane anaesthesia glucose turnover must have been greatly increased whereas from about 0.5h after induction it was decreased.

Anesthesia, Inhalation↗
PubMed2003

Effects of halothane and sevoflurane on QT dispersion in paediatric patients.

BACKGROUND: The QT dispersion (QTd) of the ECG is an indirect measure of heterogeneity of ventricular repolarization which may contribute to complex ventricular arrhythmias. We compared the effects of halothane and sevoflurane on QTd, and heart-rate corrected QT dispersion (QTcd). METHODS: Fifty ASA physical status I patients, aged 5-15 years, undergoing general anaesthesia were studied. A control ECG recording was printed before induction of anaesthesia. In the halothane group, anaesthesia was induced with halothane 4% in 2 : 1 ratio of air : O2 mixture and in the sevoflurane group with sevoflurane 8% in 2 : 1 ratio of air : O2 mixture. The ECG was recorded 1 and 3 min after induction of anaesthesia, 1 and 3 min after the administration of vecuronium 0.08 m.kg(-1) intravenous and 1 and 3 min after the tracheal intubation. All ECGs were analysed by two cardiologists blinded to the anaesthetic. RESULTS: Although QTd increased in both groups following intubation, this difference was not statistically significant when compared with control values. Following intubation five patients in the halothane group had ventricular arrhythmias of short duration, whereas no arrhythmias were recorded in the sevoflurane group (P = 0.052). Following intubation, QTd (45 +/- 15 ms vs 40 +/- 14 ms) and QTcd (60 +/- 17 ms vs 55 +/- 16 ms) values in the halothane group were significantly greater than the sevoflurane group (P < 0.05). CONCLUSION: Neither sevoflurane nor halothane caused a significant increase in QTd compared with control values before induction. Only QTd following intubation was significantly greater in the halothane group than the sevoflurane group.

Adolescent↗
PubMed2004

The correlation between bispectral index and airway reflexes with sevoflurane and halothane anaesthesia.

BACKGROUND: Unwanted airway reflexes such as laryngospasm are a frequent cause for concern in paediatric anaesthesia. They are more active during light anaesthesia. Bispectral index (BIS) is a recognized measure of anaesthetic effect. Ensuring adequate depth with the BIS may prevent these reflexes. This study investigates the relationship between BIS and a defined measure of airway reactivity. METHODS: Sixty-two children scheduled for direct laryngoscopy and bronchoscopy were enrolled in this prospective nonrandomized blinded study. They were induced and maintained with either sevoflurane or halothane. When depth of anaesthesia was judged deep enough on clinical grounds, the cords were sprayed with 2% lidocaine. Using an A2000 monitor, the BIS was recorded at the moment of spraying the cords. The anaesthetist was blinded to the BIS and noted whether or not spraying resulted in complete closure of the cords. Breath holding, desaturation and coughing were also recorded as secondary endpoints. RESULTS: Using logistic regression there was a significant correlation between BIS and cord closure for halothane but not for sevoflurane (halothane Pseudo r2 = 0.5, P = 0.003; sevoflurane Pseudo r2 = 0.0004, P = 0.9). Although the study was not specifically designed to test for it, no difference was detected between agents in the incidence of cord closure (halothane 38%, sevoflurane 36%), or secondary endpoints (halothane 29%, sevoflurane 29%). CONCLUSIONS: The BIS may be useful to help prevent unwanted airway reflexes when using halothane but not with sevoflurane. The differing sites of anaesthetic action for sevoflurane and halothane may explain this result.

Adolescent↗
PubMed2004

Magnesium deficiency alters the threshold for epinephrine-induced arrhythmias during halothane or sevoflurane anesthesia in the rat.

OBJECTIVE: To determine the effect of chronic magnesium (Mg2+) deficiency on the relative arrhythmogenicity of halothane and sevoflurane in the rat. DESIGN: Prospective, randomized, nonblinded study. SETTING: University laboratory. PARTICIPANTS: Male Sprague-Dawley rats (n = 48). INTERVENTIONS: Rats were maintained on a Mg2+-deficient or control diet for 14 days, at which time they were anesthetized with halothane or sevoflurane, a tracheostomy was performed, and the lungs were ventilated to maintain normocapnia. Catheters were inserted into a femoral vein and carotid artery. Lead II of the electrocardiogram was monitored to determine the threshold for epinephrine-induced arrhythmias. MEASUREMENTS AND MAIN RESULTS: Chronic Mg2+ deficiency significantly decreased the dose of epinephrine required for arrhythmias (ADE). The reduction in the ADE was approximately one third during halothane anesthesia (p < 0.05) and one fifth during sevoflurane anesthesia (p < 0.001). Infusion of magnesium sulphate completely reversed the reduction in ADE. In normomagnesemic rats, the halothane ADE was significantly less than the sevoflurane ADE (mean difference = 6.0 microg/kg, 95% confidence interval of the difference = 3.6 to 8.4 microg/kg) (p < 0.005). Mg2+ deficiency significantly attenuated the difference between the halothane ADE and the sevoflurane ADE (mean difference in the Mg2+-deficient group = 0.6 microg/kg, 95% confidence interval of the difference = -0.2 to 1.5 microg/kg). CONCLUSION: Chronic Mg2+ deficiency decreased the threshold for epinephrine-induced arrhythmias and attenuated differences between the arrhythmogenic potential of halothane and sevoflurane, suggesting that arrhythmias are as likely to develop with sevoflurane as with halothane in the presence of coexisting magnesium deficiency and elevated catecholamines.

Anesthesia, Inhalation↗
PubMed1992

[Changes in cerebral metabolism and cerebral blood flow caused by halothane and isoflurane in increasing concentrations].

The results of two studies on the effects of halothane and isoflurane in increasing end-tidal concentrations (0.25; 0.5; 1.0vol%) on the cerebral metabolic rate for oxygen and the cerebral blood flow are compared. Both studies were performed on baboons using the same experimental model. Cerebral blood flow was determined from a washout curve after the intracarotid injection of 133xenon. Halothane and isoflurane led to a dose-dependent decrease of the cerebral metabolic rate for oxygen. Increasing concentrations of halothane caused a decrease of cerebral oxygen consumption from 3.4 +/- 0.8 (baseline) to 2.9 +/- 0.8 (0.25vol%), 2.7 +/- 0.7 (0.5vol%) and 2.4 +/- 0.4 mlO2 100 g-1min-1 at 1.0vol%. The administration of isoflurane reduced the cerebral oxygen consumption significantly from baseline 3.7 +/- 1.0 to 2.9 +/- 0.9 at 0.25vol%, 2.6 +/- 0.6 at 0.5vol% and 1.8 +/- 0.8 mlO2 100 g-1min-1 with 1.0vol%. A significant, dose-independent reduction of the cerebral blood flow from 55.8 +/- 8.0 to 46.3 +/- 10.2 (0.25%) to 44.6 +/- 9.5 (0.5vol%) and 44.5 +/- 10.2 ml 100 g-1min-1 (1.0vol%) was observed with halothane. However, a dose-dependent decrease in calculated cerebrovascular resistance was seen at 1.0vol% of halothane. If mean arterial pressure was kept within the normal limits of cerebrovascular autoregulation by the administration of angiotensin-II-amid during 1.0vol% of halothane a marked increase in cerebral blood flow above the baseline value was observed. The lacking increase in cerebral blood flow observed at 1.0vol% of halothane without blood pressure support appeared to be caused by the low cerebral perfusion pressure rather than by vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Manipulation of the radiosensitivity of pig epidermis by changing the concentration of oxygen and halothane in the anaesthetic gas mixture.

A gas mixture of halothane, oxygen and nitrous oxide has been used to anesthetize pigs for irradiation. The effects of various concentrations of halothane and oxygen on the radiosensitivity of the epidermis were examined after irradiation with single doses of beta-rays from strontium-90 plaques. The incidence of moist desquamation was used as an endpoint, and experiments were compared on the basis of the dose associated with a 50 per cent incidence of moist desquamation (ED50 +/- SE). For pigs inspiring an anaesthetic gas mixture of 2 per cent halothane, approximately 70 per cent oxygen and approximately 30 per cent nitrous oxide the ED50 for moist desquamation was 27.32 +/- 0.52 Gy. A similar ED50 value of 27.39 +/- 1.20 Gy was obtained when 4 per cent halothane was used in place of 2 per cent. When the pigs were breathing air (approximately 21 per cent oxygen) in place of oxygen and nitrous oxide the ED50 values were increased significantly to 31.25 +/- 0.94 Gy and 33.72 +/- 1.08 Gy for 2, and 4 per cent halothane, respectively. This change in the radiosensitivity of the epidermis was represented by dose modification factors of approximately 1.13 and approximately 1.23 for 2 and 4 per cent halothane, respectively. Irradiation with a high oxygen concentration in the inspired gas mixture did not result in any significant variation of the dose required to produce moist desquamation in 50 per cent of the fields irradiated for dorsal, lateral and ventral positioned skin fields on the flank. However, pigs breathing air and halothane during irradiation showed marked differences in the radiosensitivity of the various sites on the flank, with ED50 values for moist desquamation of approximately 37 Gy and 26-30 Gy for dorsal and ventral positioned fields, respectively. This marked difference in radiosensitivity suggests variations in the physiological compensation over the flank when pigs are breathing oxygen at low concentrations under anaesthesia.

Anesthesia, Inhalation↗
PubMed1974

The effects of halothane on cultured mouse neuroblastoma cells. I. Inhibition of morphological differentiation.

Mouse neuroblastoma cells (clone NB2a) were cultured in the presence of 0.3-2.1% halothane in the gas phase for up to 72 h. Halothane inhibited neurite extension dose dependently and virtually abolished microspike formation even at the lowest concentration tested. These effects were completely reversible. Electron microscopy demonstrated that microfilaments measuring 40-80 A in diameter are the only fibrous organelles visible within microspikes. When the cells were exposed to halothane, no microfilamentous complexes could be identified in any cells and the subcortical regions of neurites often appeared devoid of individual microfilaments. Microtubules were still present in neurites after exposure to halothane concentrations at which microfilaments disappeared. However, at concentrations above 1.0%, microtubules gradually appeared to decrease in number. Short-term experiments showed that existing neurites and microspikes rapidly retracted when suddenly exposed to culture medium equilibrated with 1.0% halothane and quickly reformed when the halothane was removed. The inhibition of neuroblastoma cell differentiation by halothane appears to be mediated by disruption of 40-80 A diameter microfilaments.

Animals↗
PubMed1985

Rapid induction of halothane anaesthesia in man.

The cardiopulmonary and anaesthetic responses of nine healthy volunteers, breathing concentrations of 1-4% halothane in oxygen, were studied. Supine fasting subjects breathing room air exhaled to residual volume and then inhaled a vital capacity breath of 1, 2, 3 or 4% halothane in oxygen. After a breath-hold of 30-90 s they exhaled and then breathed spontaneously the same anaesthetic mixture for up to 2 min. The electrocardiogram, arterial pressure, heart sounds and arterial oxygen saturation, were monitored, and respiratory gases were analysed by mass spectrometry. The maximum effect was seen after breathing 4% halothane. All volunteers were amnesic after the first breath and unresponsive to command after 2 min. Little or no excitement occurred. A maximum decrease of 12 mm Hg in systolic pressure was seen while breathing 4% halothane. Bradycardia, hypoxia and clinically important hypercarbia did not occur. At all inspired concentrations of halothane, the end-tidal halothane concentration increased rapidly and was 30% of the inspired value after 1 min. No volunteer found this technique to be unpleasant. Rapid induction of general anaesthesia with 2-4% halothane in oxygen is effective, safe and well accepted by healthy young adults.

Adult↗
PubMed1991

Arterial washin of halothane and isoflurane in young and elderly adult patients.

We have studied the effect of age on washin of isoflurane and halothane by comparing end-tidal (PE') and arterial (Pa) partial pressures of the agents in young (18-32 yr) and elderly (63-82 yr) healthy patients for 20 min after introduction of the agents, before surgery. PE' was measured by infra-red analysis and Pa by gas chromatography. Washin of isoflurane occurred at the same rate in the young and elderly, with no significant difference between young and elderly in PE' or Pa as proportions of the inspired partial pressure (PI). After 20 min of isoflurane administration, mean Pa/PI in the young was 0.57 (95% confidence limit (CL) 0.53-0.62) and 0.55 in the elderly (95% CL 0.51-0.59). Washin of halothane was slower in the elderly than in the young, with Pa/PI significantly less in the elderly from 10 min after introduction of halothane. The difference between age groups, however, was small: mean Pa/PI after 20 min of halothane administration 0.45 (95% CL 0.41-0.49) in the young and 0.38 (95% CL 0.35-0.41) in the elderly. Washin of isoflurane was significantly faster than that of halothane in both young and elderly subjects. For isoflurane, the PE'-Pa gradient was small relative to Pa and did not differ significantly between young and elderly. For halothane, PE'-Pa in the young did not differ significantly from that for isoflurane. In the elderly, PE'-Pa for halothane was significantly greater than in the young and than PE'-Pa for isoflurane.

Adolescent↗
PubMed1993

Effect of a sub-anaesthetic concentration of halothane on the ventilatory response to sustained hypoxia in healthy humans.

We selected nine normal subjects (8M, 1F; aged 25-43 yr) with brisk hypoxic ventilatory responses, and studied their ventilatory response to sustained isocapnic hypoxia (SaO2 82 (SEM 0.1) % for 25 min) in the presence and absence of 0.1% inspired halothane. Halothane had no significant effect on baseline ventilation or gas exchange. In the absence of halothane, ventilation increased initially from mean 7.57 (0.35) litre min-1 to 14.54 (0.91) litre min-1, and decreased subsequently to 10.74 (0.32) litre min-1 during hypoxia (both P < 0.05). In the presence of 0.1% inspired halothane, ventilation increased initially from 7.19 (0.47) litre min-1 to 12.08 (0.99) litre min-1 (P < 0.05), then decreased to 10.12 (0.28) litre min-1 during sustained hypoxia (ns compared with baseline normoxic ventilation). Halothane reduced significantly the initial increase in ventilation (P < 0.05), but did not enhance the subsequent decrease. These results confirm that a sub-anaesthetic concentration of halothane depresses the initial hypoxic ventilatory response; the response during prolonged periods of hypoxia is, however, less than the initial response and is reduced in the presence or absence of a sub-anaesthetic concentration of halothane.

Adult↗
PubMed1994

Effects of halothane and diltiazem on L-type calcium currents in single smooth muscle cells from rabbit portal veins.

We have studied the effects of halothane and diltiazem on L-type voltage-dependent calcium currents (ICa) in single smooth muscle cells from rabbit portal veins using a whole cell voltage clamp technique. The threshold of ICa was -30mV and the peak current was reached at 0mV. Halothane (0.25, 0.5, 1.0, 1.5 and 2.0%) decreased ICa in a concentration-dependent manner and shifted the ICa activation threshold to the depolarizing side. Halothane 2.0% abolished ICa. Diltiazem 10(-8)-10(-6) mol litre-1, a calcium channel antagonist, also depressed ICa in a concentration-dependent manner. Administration of both 0.5% halothane and diltiazem 10(-7) mol litre-1 (concentrations lower than the clinical therapeutic range) abolished ICa; however, halothane did not exhibit use-dependent inhibition of ICa whereas diltiazem showed partial use-dependency. We conclude that the decrease in ICa produced by halothane is associated with a direct vasodilator effect of this anaesthetic, but is not explained by block of Ca2+ channels similar to the action of diltiazem. Furthermore, administration of low concentrations of both halothane and diltiazem decreased ICa and may reduce the contractility of the vascular smooth muscle cells.

Animals↗
PubMed1995

Halothane affects ventilatory afterdischarge in humans.

In awake humans, when ventilatory stimulation is suddenly removed, the subsequent change in minute ventilation (which remains at higher levels for longer times than expected from the dynamics of the chemoreceptors) is termed ventilatory after discharge. In this study we investigated the effects of subanaesthetic concentrations of halothane on afterdischarge. The ventilatory pattern after sudden termination of brief periods (90-180 s) of isocapnic hypoxia (PE'cO2 approximately 0.1 kPa above initial resting values; PE'O2 6.5 kPa) by normoxia (PE'O2 14 kPa) was determined in healthy volunteers. Six subjects underwent 13 studies without halothane (control) and six others 10 studies during inhalation of 0.22% halothane. Isocapnic hypoxia caused a mean increase in ventilation of 10.8 (SD 2.4) litre min-1 in the control and 4.2 (2.4) litre min-1 in the halothane studies (P < 0.01). The transition to normoxia caused a slow ventilatory decay in the control and a fast decay in the halothane groups: the interval that occurred between the "last hypoxic" breath and the time required for ventilation to return to 110% of baseline was 60.7 (23) s for the control and 12.3 (6.0) s for the halothane studies (P < 0.05). Taking into consideration the different factors that determine the pattern of breathing immediately after termination of a brief period of hypoxia by normoxia (PE'O2 waveform, transport delay time between lungs and carotid bodies, time constant of the peripheral chemoreflex loop and afterdischarge), the faster ventilatory decay observed with halothane is probably related to suppression of afterdischarge.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Nitrous oxide or halothane, or both, fail to suppress c-fos expression in rat spinal cord dorsal horn neurones after subcutaneous formalin.

In rats injected s.c. with formalin, behavioural correlates of the amount and pattern of Fos-like immunoreactivity (Fos-Ll) (molecular responses to pain) were studied to test if early phase treatment with 75% nitrous oxide or 2% halothane, or both, suppressed subsequent spinal sensitization. Rats were allocated to four treatment groups: (1) 100% oxygen (control, n = 15), (2) 75% nitrous oxide (0.5 MAC, n = 12), (3) 2% halothane (1 MAC, n = 12), and (4) 75% nitrous oxide with 2% halothane (1.5 MAC, n = 18) for 20 min. Each rat then received a s.c. injection of 1% formalin 50 microliters into the left hindpaw and anaesthesia was maintained for another 5 min (early phase). A fifth group of rats receiving fentanyl 100 micrograms kg-1 (n = 12) 10 min before formalin injection were studied simultaneously as a positive control. Rats in all groups were killed 60 min after formalin injection and maximal counts of Fos-Ll labelled neurones in the dorsal horn of the rat spinal cord were compared according to laminar distribution. Formalin-induced behavioural hyperalgesia during the early phase was suppressed completely by fentanyl, 75% nitrous oxide, or 2% halothane, or both. The late phase response was attenuated by all four anaesthetic regimens within 20 min after injection, whereas behavioural scores for the nitrous oxide, halothane, or both, groups were nearly identical to the control 20 min later. Fentanyl suppressed the late phase response until 30 min after formalin injection but failed to reduce it thereafter. The numbers of Fos-Ll labelled neurones for groups given nitrous oxide, or halothane, or both, were identical to the control, whereas numbers for fentanyl were 47.2% less (P < 0.01). The decrease occurred predominantly in the neck of the dorsal horn (44.9% of control, P < 0.01) and also in the nucleus proprius and superficial laminae (54.4% and 56.2% of control, P < 0.05). In summary, we found that nitrous oxide, or halothane, or both, did not suppress subsequent spinal sensitization to noxious stimulation. This result supports the previous hypothesis that inhalation anaesthesia lacks pre-emptive analgesic action. Inhalation anaesthetic agents, unlike fentanyl, suppress the early and late phase response because of anaesthetic but not analgesic effects. Thus, we suggest that measuring the genetic product of c-fos proto-oncogene is a useful adjunct to pharmacological tests whenever behavioural hyperalgesia is questionable or unobtainable.

Anesthetics, Inhalation↗
PubMed1996

Effect of halothane, isoflurane and desflurane on lower oesophageal sphincter tone.

We have studied the effects of volatile anaesthetics on lower oesophageal sphincter (LOS) tone in three groups of eight pigs allocated randomly to receive end-tidal concentrations of 0.5, 1.0 and 1.5 MAC of desflurane, isoflurane or halothane for 15 min. LOS and oesophageal barrier pressures (BrP = LOSP - gastric pressure) were measured using a manometric method. The decrease in BrP paralleled the decrease in LOS pressure and was significant at 0.5 MAC for isoflurane and at 1.0 MAC for halothane. At 1.5 MAC, BrP values were approximately 62% of baseline values for halothane, 37% for isoflurane and 83% for desflurane. Inter-group comparisons showed that BrP did not differ at baseline and at 0.5 MAC. At 1.0 MAC the effect of isoflurane on BrP was significantly different from desflurane (P < 0.001) and halothane (P < 0.02) whereas the effect of desflurane on BrP was not significantly different from halothane. At 1.5 MAC the effect of isoflurane on BrP was significantly different from desflurane (P < 0.01) and halothane (P < 0.05) whereas the effect of desflurane on BrP was not significantly different from halothane. We conclude that desflurane maintained BrP and this may be clinically important in patients at high risk of regurgitation.

Anesthetics, Inhalation↗
PubMed1997

Rapid inhalation induction in children: 8% sevoflurane compared with 5% halothane.

Sevoflurane has a lower blood-gas solubility and a less pungent odour than halothane; this may allow more rapid induction of anaesthesia. In a randomized, blinded study, we compared the induction characteristics of maximum initial inspired concentration of 8% sevoflurane and 5% halothane using conventional vaporizers in children aged 3 months to 3 years. There was no statistically significant difference in induction times between the two groups: mean times to loss of consciousness were 1 min 12 s (SD 18 s, range 40 s-1 min 44 s) for sevoflurane and 1 min 16 s (SD 17 s, range 50 s-1 min 52 s) for halothane, although these times were shorter than in previous studies using a gradual increase in vapour concentration. A small number of complications were noted in both groups, although none interfered with induction of anaesthesia. Struggling scores were lower in the sevoflurane group than in the halothane group (chi-square for trends = 6.34, P < 0.02). A significant number (11 of 15) of parents of children in the sevoflurane group who had previous experience of halothane induction preferred sevoflurane (chi-square for trends = 4.03, P < 0.05). We conclude that with this technique, induction was rapid with both sevoflurane and halothane. Our assessment of patient struggling and parents' perceptions suggests that induction with sevoflurane was more pleasant than with halothane.

Anesthesia, Inhalation↗