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PubMed1994

Effect of xylazine and ketamine on the pharmacokinetics of alfentanil during halothane anaesthesia.

We measured plasma concentrations of alfentanil in two horses after three different randomly ordered treatments. Each horse received halothane in oxygen by mask followed by a bolus dose of alfentanil 60 micrograms kg-1 i.v., halothane in oxygen by mask followed by an i.v. alfentanil infusion for 120 min and xylazine and ketamine followed by halothane and a bolus dose of alfentanil 60 micrograms kg-1 i.v. Halothane was maintained at 1.05-1.07% end-tidal concentration with a PaCO2 of 6-7.3 kPa. The plasma concentration-time curves were similar after bolus and infusion doses of alfentanil with halothane and could be fitted to a two-compartment open model. A plateau was noted in the plasma concentration-time curve in the presence of xylazine-ketamine which could not be modelled adequately, but suggested a three-compartment open model with an additional input component.

Alfentanil↗
PubMed1994

Influence of halothane on the effect of cAMP-dependent and cAMP-independent positive inotropic agents in human myocardium.

Volatile anaesthetics have a variety of effects on the myocardium, namely a negative inotropic effect and a catecholamine sensitizing effect. The present study was designed to see if the hydrocarbon anaesthetics interact specifically with subcellular targets of the myocardial cell, by examining the effects of halothane in the presence of positive inotropic agents with different mechanisms of action. Experiments were performed in isolated electrically driven left ventricular preparations (1 Hz, 37 degrees C, Ca2+ 1.8 mmol litre-1) from human hearts obtained at cardiac surgery. The concentration-response curves of noradrenaline, milrinone, BayK 8644 and Ca2+ were investigated in the absence and in the presence of halothane. Halothane enhanced the efficacy of noradrenaline and milrinone but not of Ca2+ or BayK 8644. The potency of milrinone was also increased by halothane, whereas the potency of BayK 8644 was decreased and those of noradrenaline and Ca2+ were unchanged. Halothane differentially influences the effects of agents with different positive inotropic mechanisms. This experimental approach can be taken as a functional method to localize the mechanisms of action of the inhalation anaesthetics in human myocardium, namely sensitization of cAMP formation and interaction with L-type Ca2+ channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1995

Comparison of the effects of sevoflurane, isoflurane and halothane on indocyanine green clearance.

We have examined the effects of inhalation anaesthetics on indocyanine green (ICG) clearance, as an index of hepatic function, in patients undergoing elective surgery. Recently, a new method has been developed to measure in real-time the disappearance rate of ICG from plasma. This method eliminates the multiple sampling and delay of the conventional ICG test. ICG clearance is displayed as two indices: K (ICG disappearance rate) and R15 (ICG retention rate 15 min after injection of ICG 0.5 mg kg-1). This measurement was performed in patients before and after 1 MAC of sevoflurane (n = 6), 2 MAC of sevoflurane (n = 6), 1 MAC of isoflurane (n = 6), 2 MAC of isoflurane (n = 6), 1 MAC of halothane (n = 6) or 2 MAC of halothane (n = 6) without surgical stress. Although mean arterial pressure decreased significantly at 1 and 2 MAC of sevoflurane, 2 MAC of halothane, and 1 and 2 MAC of isoflurane, ICG clearance was maintained at awake levels, except at 2 MAC of halothane (K = mean-33 (sem 3)%, R15 = +90 (3)% from awake values). We conclude that sevoflurane and isoflurane have a more favourable effect on liver circulation than halothane.

Adult↗
PubMed1995

Do nitrous oxide and halothane influence opioid receptor binding in SH-SY5Y human neuroblastoma cells?

The site of interaction of opioids and inhalation anaesthetic agents is unknown, but may be at the level of the opioid receptor. In this study we have used SH-SY5Y human neuroblastoma cells, which express both mu and delta receptors, to examine the effects of halothane on the receptor binding profiles of [3H]diprenorphine (DPN), an opioid receptor antagonist, and [3H] [D-Ala2,MePhe4, Gly(ol)5]enkephalin (DAMGO), a mu receptor selective agonist. Binding of [3H]DPN and [3H]DAMGO was performed at 37 degrees C for 60 min in the presence of air, nitrous oxide (75%) or air containing halothane (0.5-5.0% v/v). Compared with air controls, neither 75% nitrous oxide nor 0.5, 1.0, 2.0 and 5.0% halothane influenced DPN binding variables. Binding of [3H]DAMGO was unaffected by 1.0% halothane, but 5.0% halothane reduced the affinity, with a modest increase in Kd (1.15 (0.16) to 1.7 (0.2) nmol litre-1) without effect on Bmax. Our data suggest that the site of opioid and volatile anaesthetic interaction is not at the opioid receptor.

Analgesics↗
PubMed1996

Differential effects of desflurane and halothane on peripheral airway smooth muscle.

Volatile anaesthetics have been shown to have direct relaxant effects on airway smooth muscle. We have examined the effects of 0.9, 1.9, and 2.8 dog MAC of desflurane and halothane on isolated proximal and distal canine airways precontracted with acetylcholine. The proximal and distal airway smooth muscle relaxed with increasing concentration of each anaesthetic in a dose-related manner. Desflurane had a greater relaxant effect than halothane on the proximal airway only at 2.8 MAC. Desflurane relaxed the distal airway to a greater extent than halothane at 1.9 and 2.8 MAC. The distal airway smooth muscle was more sensitive to volatile anaesthetics than the proximal airway smooth muscle with either halothane or desflurane at all concentrations tested. This effect may be a result of differences in cartilage content, myosin content, epithelium-dependent effects, receptor density, myofilament sensitivity to Ca2+, sarcoplasmic reticulum Ca2+ control, or ionic fluxes in the proximal airway compared with the distal airway. The increased sensitivity of airway smooth muscle to desflurane compared with halothane is not known but may be related to possible differences in the effects of Ca2+ homeostasis.

Acetylcholine↗
PubMed1996

Role of prostaglandins and nitric oxide on halothane-induced arteriolar dilatation in rat diaphragm.

The effects of anaesthetics on the microcirculation of the diaphragm are incompletely understood. Therefore, we assessed by in vivo intravital microscopy in rats the action of halothane on diaphragmatic arteriolar diameter and the role of nitric oxide and prostaglandins on halothane-induced diaphragmatic arteriolar diameter. We studied 54 rats anaesthetized with thiopentone. Dose-response curves to topically applied Krebs' solution saturated with halothane at increasing concentrations of 0%, 1%, 3% and 5% were carried out in the presence of an inhibitor of nitric oxide synthesis (N omega-nitro-L-arginine (LNA), 300 mumol litre-1) or inhibitors of prostaglandin synthesis (mefenamic acid 20 mumol litre-1 or indomethacin 20 mol litre-1) or in the absence of any inhibitor. We found dose-dependent arteriolar dilatation which was abolished by mefenamic acid and indomethacin. In contrast, the effect of halothane was not modified by LNA. These data demonstrated that halothane-induced arteriolar dilatation in the diaphragm of the rat was mediated by prostaglandins but not by nitric oxide.

Anesthetics, Inhalation↗
PubMed1997

Comparison of induction and recovery between sevoflurane and halothane supplementation of anaesthesia in children undergoing outpatient dental extractions.

We have compared sevoflurane and halothane in a double-blind controlled study for supplementation of nitrous oxide and oxygen anaesthesia in 80 children undergoing dental extraction as outpatients. Induction of anaesthesia was more rapid in those who received sevoflurane compared with those who received halothane (89 s compared with 127 s for loss of eyelash reflex). In both groups, mean duration of administration of anaesthesia was less than 4 min. Those who received sevoflurane were slower to awaken (167 s compared with 102 s), although discharge times from hospital were similar. The incidence of complications during induction and maintenance was low in both groups and return to normal appetite and activity occurred in the majority of children on the same day. More children who received halothane suffered nausea after leaving hospital. We conclude that sevoflurane is a suitable alternative to halothane, with more rapid induction of anaesthesia, but in these short procedures, awakening time was slower than after halothane.

Ambulatory Surgical Procedures↗
PubMed1997

Comparison of sevoflurane and halothane for outpatient dental anaesthesia in children.

In a prospective, randomized, double-blind clinical study, we have studied 100 children, aged 2-12 yr, to compare halothane and sevoflurane in outpatient dental anaesthesia. All patients were unpremedicated and received inhalation induction using nitrous oxide in oxygen supplemented with either halothane (maximum inspired concentration 5%) or sevoflurane (maximum inspired concentration 8%). Time to loss of the eyelash reflex was more rapid using sevoflurane although time to adequate anaesthesia (to allow insertion of a mouth prop) was slower in the sevoflurane group. The incidence of cardiac arrhythmia was higher during halothane (62%) than during sevoflurane anaesthesia (28%) (P < 0.005) and the arrhythmias were more often ventricular in origin. The two agents were comparable in terms of ease of use and quality of anaesthesia, and times to eye opening and satisfying discharge criteria were similar. We conclude that sevoflurane has qualities that have made halothane the most used inhalation agent for children, and that it is superior to halothane in dental outpatients where cardiac arrhythmias are a particular problem.

Ambulatory Surgical Procedures↗
PubMed1998

Comparison of the effects of sevoflurane, isoflurane and halothane on rat myocardium.

The effects of sevoflurane on myocardial contraction and relaxation are poorly understood. Therefore, we studied the effects of equianaesthetic concentrations (0.5, 1, 1.5, 2 and 2.5 MAC) of sevoflurane, isoflurane and halothane on inotropic and lusitropic (myocardial relaxation) variables, and post-rest potentiation in rat left ventricular papillary muscles in vitro. Sevoflurane and isoflurane caused comparable concentration-dependent negative inotropic effects which were significantly lower than those induced by halothane (P < 0.05). Sevoflurane and isoflurane did not modify lusitropic variables under low or high load, whereas halothane showed a negative lusitropic effect at high concentrations. Halothane suppressed post-rest potentiation, whereas isoflurane and sevoflurane did not. Post-rest recovery was unaffected by halothane, isoflurane or sevoflurane at any concentration. Thus in rat myocardium, sevoflurane and isoflurane caused comparable negative inotropic effects, had no significant lusitropic effects and did not alter post-rest potentiation, suggesting that they did not significantly modify the functions of the sarcoplasmic reticulum.

Anesthetics, Inhalation↗
PubMed1998

Comparison of the effects of halothane, isoflurane and methoxyflurane on the electroencephalogram of the horse.

We have investigated in eight ponies the effects of three different end-tidal concentrations of halothane, isoflurane and methoxyflurane on median (F50) and 95% spectral edge (F95) frequencies of the EEG and the second differential (DD) of the middle latency auditory evoked potential (MLAEP). The three concentrations of each agent were chosen to represent approximately the minimum alveolar concentration (MAC), 1.25 MAC and 1.5 MAC for each agent. During halothane anaesthesia, F95 decreased progressively as halothane concentration increased, from mean 13.9 (SD 2.6) at 0.8% to 11.9 (1.1) at 1.2%. DD was lower during anaesthesia with the highest concentration (21 (6.5)) compared with the lowest (27.6 (11.4)). There were no significant changes in F50. During isoflurane anaesthesia, there was a small, but significant increase in F95 between the intermediate and highest concentrations (10.2 (1.5) to 10.8 (1.6)). There were no changes in F50 and DD. Values of F95, F50 and DD at all isoflurane concentrations were similar to those of halothane at the highest concentration. During methoxyflurane anaesthesia, F95 and F50 decreased progressively as methoxyflurane concentration was increased, from 21.3 (0.7) and 6.5 (1), respectively, at 0.26%, to 20.1 (0.6) and 5.6 (0.8), respectively, at 0.39%. DD was lower during anaesthesia with the highest concentration of methoxyflurane (25.7 (7.8)) compared with the lowest (39.7 (20.6)). Values of F95, F50 and DD at all methoxyflurane concentrations were higher than those seen with halothane at the lowest concentration. The different relative positions of the dose-response curves for EEG and MLAEP changes compared with antinociception (MAC) changes suggest differences in the mechanisms of action of these three agents. These differences may explain the incomplete adherence to the Meyer-Overton rule.

Anesthetics, Inhalation↗
PubMed2000

Water vapour in a closed anaesthesia circuit reduces degradation/adsorption of halothane by dried soda lime.

Dry lime causes a loss of volatile anaesthetics by degrading and adsorbing them. Degradation produces toxic substances and heat. Rehydration of lime stops degradation. If humidified breathing gases rehydrate lime, closed anaesthesia-circuits may reduce the loss of anaesthetics. To test this hypothesis we ventilated a reservoir bag with PhysioFlex-devices using fresh (F) and dried (D) soda lime both in the presence (+H) and absence (-H) of halothane. We measured halothane delivery, humidity, temperature, and lime weight. Halothane was lost for 13 min in D + H. Humidity increased steeper with fresh lime, whereas absorbent weight increased more with dried lime; halothane increased both variables (F + H: 99%, 8 g; F - H: 93%, 6 g; D + H: 58%, 17 g; D - H: 24%, 15 g). Surprisingly, temperature remained constant, probably because of the high gas flow (70 litres min-1) generated inside the Physioflex. These findings indicate rehydration of dried lime by humid gases and a rapid cessation of the loss of halothane in the PhysioFlex.

Adsorption↗
PubMed2000

Halothane and desflurane requirements in alcohol-tolerant and -nontolerant rats.

On the basis of data implicating GABAA receptors in the effects of volatile general anaesthetics, we hypothesized that alcohol-, barbiturate-, and benzodiazepine-sensitive alcohol-nontolerant (ANT) rats would also be more sensitive than alcohol-tolerant (AT) rats to two clinical general anaesthetics with differing potencies, halothane and desflurane. The obtunding effect of halothane and desflurane on mature ANT (n = 17) and AT (n = 16) rats was assessed by the loss-of-righting reflex endpoint. ANT rats were significantly (P < 0.0001) more sensitive to the obtunding effects of both halothane and desflurane (ED50 = 0.45 +/- 0.03% atm for ANT vs 0.95 +/- 0.04% atm for AT and 2.16 +/- 0.17 vs 3.69 +/- 0.13% atm, respectively). The immobilization effect of halothane and desflurane was assessed with the tail clamp/withdrawal endpoint. ANT rats were more sensitive to the effects of halothane (ED50 = 1.10 +/- 0.08% atm for ANT vs 1.72 +/- 0.09% atm for AT; P < 0.0001) but not desflurane (ED50 = 6.25 +/- 0.25% atm for ANT vs 5.85 +/- 0.21% atm for AT). The data presented support the hypothesis that volatile anaesthetics interact with specific neuronal proteins (possibly GABAA receptors) and agree with recent hypotheses that different elements of the anaesthetic state are produced by separate sites or mechanisms.

Anesthetics, Inhalation↗
PubMed2005

Differential effects of halothane and isoflurane on lumbar dorsal horn neuronal windup and excitability.

BACKGROUND: Windup of spinal nociceptive neurones may underlie temporal summation of pain, influencing the minimum alveolar concentration (MAC) of anaesthetics required to prevent movement to supramaximal stimuli. We hypothesized that halothane and isoflurane would differentially affect windup of dorsal horn neurones. METHODS: We recorded 18 nociceptive dorsal horn neurones exhibiting windup to 1 Hz electrical hindpaw stimuli in rats. Effects of 0.8 and 1.2 MAC isoflurane and halothane were recorded in the same neurones (counterbalanced, crossover design). Windup was calculated as the total number of C-fibre (100-400 ms latency) plus afterdischarge (400-1000 ms latency) spikes/20 stimuli (area under curve, AUC) or absolute windup (C-fibre plus afterdischarge-20 x initial response). RESULTS: Increasing isoflurane from 0.8 to 1.2 MAC did not affect AUC, but increased absolute windup from 429 (62) to 618 (84) impulses/20 stimuli (P<0.05) and depressed the initial C-fibre response from 14 (3) to 8 (2) impulses (P<0.05). Increasing halothane from 0.8 to 1.2 MAC depressed AUC from 690 (79) to 537 (65) impulses/20 stimuli (P<0.05) and the initial response from 18 (2) to 13 (2) impulses (P<0.05), but absolute windup was not affected. Absolute windup was 117% greater during 1.2 MAC isoflurane compared with 1.2 MAC halothane. CONCLUSIONS: Windup was significantly greater under isoflurane than halothane anaesthesia at 1.2 MAC, whereas the initial C-fibre response was suppressed more by isoflurane. These findings suggest that these two anaesthetics have mechanistically distinct effects on neuronal windup and excitability.

Action Potentials↗
PubMed2000

Halothane attenuates the endothelial Ca2+ increase and vasorelaxation of vascular smooth muscle in the rat aorta.

Isolated spiral strips of rat thoracic aorta with endothelium were suspended for isometric tension recordings in a physiological salt solution. Endothelium-dependent vasorelaxation was elicited by carbachol 10(-6) and 10(-5) mol litre-1 during norepinephrine-induced contractions, and the effects of 1.5% and 3% halothane were evaluated with concomitant measurement of [Ca2+]i using fura-2-Ca2+ fluorescence. The effects of halothane on endothelium-dependent relaxation were compared with those of nitro G-L-arginine methyl ester 10(-4) mol litre-1 (L-NAME: an inhibitor of nitric oxide synthase). Carbachol reduced norepinephrine-induced contractions in a concentration-dependent manner, but augmented the norepinephrine-induced increase in [Ca2+]i in endothelium intact strips. In contrast, carbachol did not influence muscle tension or [Ca2+]i when the endothelium was completely denuded. Although 3% halothane and L-NAME 10(-4) mol litre-1 inhibited carbachol-induced vasorelaxation in a similar manner, halothane inhibited carbachol-induced increases in [Ca2+]i. These results indicate that halothane inhibited a carbachol-induced increase in [Ca2+]i in the endothelium, which subsequently attenuated the decrease in muscle tension.

Anesthetics, Inhalation↗
PubMed1995

Rate of anterior chamber aqueous formation, trabecular outflow facility, and intraocular compliance during desflurane or halothane anesthesia in dogs.

The present study examined the effects of desflurane on intraocular pressure (IOP), the rate of anterior chamber aqueous formation, trabecular outflow facility, and intraocular compliance. The effects of desflurane were compared to those of halothane because the effects of halothane on intraocular fluid dynamics are well known. Twenty-two dogs were anesthetized for surgical preparation. Pancuronium was given intravenously to produce neuromuscular blockade, and the lungs were mechanically ventilated through a tracheal tube. After surgical preparation, anesthesia was maintained in Group 1 (n = 12) with halothane (0.8% expired) and in Group 2 (n = 10) with desflurane (7.0% expired). In both groups a series of intraocular infusions was made via a 30-gauge needle in the anterior chamber and IOP, aqueous formation, outflow facility, and intraocular compliance were determined. In Group 1 (halothane) IOP was 9.4 +/- 2.8 mm Hg (mean +/- SD), aqueous formation was 1.45 +/- 0.45 microL/min, outflow facility was 0.091 +/- 0.054 microL.min-1.mm Hg-1, and compliance was 377 +/- 282 nL/mm Hg. In Group 2 (desflurane) IOP was 11.3 +/- 3.8 mm Hg, aqueous formation was 1.61 +/- 0.56 microL/min, outflow facility was 0.097 +/- 0.062 microL.min-1.mm Hg-1, and compliance was 432 +/- 238 nL/mm Hg. These values did not differ between groups. It is concluded that in dogs aqueous humor dynamics during desflurane anesthesia are similar to those during halothane anesthesia.

Anesthesia↗
PubMed1995

Biochemical characterization of the stimulatory effects of halothane and propofol on purified brain protein kinase C.

Halothane and propofol stimulate activation of protein kinase C (PKC) in the presence of physiologically relevant lipid bilayer vesicles in vitro. The mechanism of this stimulation was characterized by analyzing the effects of halothane and propofol on the activation of purified rat brain PKC by its three essential activators, phosphatidylserine, diacylglycerol, and Ca2+, each of which is known to interact with the regulatory domain. Clinically relevant concentrations of halothane (2.4 vol%) and propofol (200 microM) increased the Vmax without affecting the Km for phosphorylation of the artificial substrate histone H1 by PKC, and increased the sensitivity of PKC to activation by phosphatidylserine, diacylglycerol, and Ca2+. Halothane reduced the EC50 values for phosphatidylserine from 18 +/- 2.5 to 11 +/- 0.6 mol% (P < 0.05), for diacylglycerol from 1.6 +/- 0.3 to 0.87 +/- 0.2 mol% (P < 0.05) and for free Ca2+ from 4.5 +/- 1.0 to 2.8 +/- 0.4 microM (P < 0.05). Propofol reduced the EC50 values for phosphatidylserine from 18 +/- 1.9 to 11 +/- 1.2 mol% (P < 0.01), for diacylglycerol from 2.5 +/- 0.3 to 1.2 +/- 0.4 mol% (P < 0.01) and for free Ca2+ from 2.8 +/- 0.7 to 1.9 +/- 0.2 microM (P < 0.05). The IC50 values for inhibition of PKC activity by the regulatory domain-specific PKC inhibitor sphingosine were increased from 20 +/- 1.5 to 26 +/- 0.6 microM (P < 0.01) by halothane and from 24 +/- 4.8 to 34 +/- 4.8 microM (P < 0.05) by propofol.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics, Inhalation↗
PubMed1996

Halothane resistance in Drosophila melanogaster: development of a model and gene localization techniques.

Studying genetically altered animals that are resistant to inhaled anesthetics may ultimately lead to an understanding of anesthetics' mechanism(s) of action. We studied the genetics of halothane resistance in a strain of Drosophila melanogaster that showed substantially increased resistance to halothane anesthesia. We developed a test method that allowed us to repeatedly observe several samples of flies exposed to the same concentration of halothane, and we measured halothane resistance. The 50% effective dose (ED50) of 91R flies (our resistant population) was greater than the ED50 of Canton-S (our control strain) by 69% in females and by 48% in males. By assessing the contributions of the three major chromosomes of Drosophila to resistance, this study found that the X and third chromosomes of 91R have no effect on resistance, while the second chromosome has a major impact. Resistance within the second chromosome was further localized by testing marked recombinant chromosomes. The central region of 91R's second chromosome, bounded by the genes for black thoracic color and cinnabar eye color, determined most if not all of the increase in resistance. We were not able to further localize resistance within this segment of the second chromosome (containing about 8% of the total genetic map distance). An autosomal dominant gene for halothane resistance in 91R was localized to a small region of the second chromosome.

Anesthetics, Inhalation↗
PubMed1996

Isoflurane and halothane produce similar alterations in aortic distensibility and characteristic aortic impedance.

The effects of volatile anesthetics on arterial mechanical properties in vivo are incompletely understood. The present investigation tested the hypothesis that isoflurane and halothane cause differential actions on the mechanical characteristics of the aorta in barbiturate-anesthetized dogs instrumented for measurement of aortic blood pressure, blood flow, and diameter. Aortic distensibility and characteristic aortic impedance were calculated from aortic diameter measurements. Oscillatory (Wo) and mean (Wm) hydraulic power were determined from aortic pressure and blood flow waveforms. Hemodynamics and aortic pressure, blood flow, and diameter were recorded before, during, and after 0.5, 0.75, and 1.0 minimum alveolar anesthetic concentration (MAC) (end-tidal) isoflurane (n = 7), or halothane (n = 8). Isoflurane and halothane caused significant (P < 0.05) and dose-related decreases in heart rate, mean arterial pressure, peak and end-diastolic aortic diameters, and aortic distensibility (e.g., from 0.16% +/- 0.03% during control to 0.24% +/- 0.04% mm Hg during 1.0 MAC isoflurane). Characteristic aortic impedance remained unchanged by either drug. In contrast to the findings with isoflurane, halothane increased the ratio of Wo to Wm (from 6.7 +/- 1.1 during control to 11.3 +/- 3.1 x 10(-2) during 1.0 MAC), suggesting that this drug decreases left ventricular mechanical efficiency. The results indicate that isoflurane and halothane do not alter characteristic aortic impedance and produce similar increases in aortic distensibility concomitant with reductions in aortic pressure. These findings support the contention that volatile anesthetic-induced alterations in aortic mechanical properties do not contribute to the differential effects of these drugs on left ventricular afterload in vivo.

Anesthetics, Inhalation↗