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PubMed1998

[Comparative study of sevoflurane and nitrous oxide versus halothane and nitrous oxide in pediatric anesthesia: efficacy and hemodynamic characteristics during induction].

OBJECTIVES: To study the efficacy, side effects and hemodynamics of anesthetic induction in pediatric patients using sevoflurane and nitrous oxide or halothane and nitrous oxide. PATIENTS AND METHODS: We studied 80 pediatric ASA I-II patients aged between 1 and 10 years old scheduled for infraumbilical surgery of short duration. The patients were randomly assigned to two groups of 40 to receive one of the two drug combinations. All the children were premedicated with nasal midazolam 0.2 mg.kg-1. Induction was by inhalation of increasing concentrations of sevoflurane or halothane. The maximum inspired concentration during induction was 7% for sevoflurane and 3% for halothane. We analyzed induction time, side effects and hemodynamic variables. RESULTS: The induction time was 2.06 +/- 0.5 min for halothane and 1.6 +/- 0.6 min for sevoflurane (p < 0.01). We observed no differences between the groups in coughing, laryngospasm, bronchospasm, secretions, apnea, nausea, vomiting, agitation or hiccoughing. Supraventricular beats appeared in 22.5% of patients in the halothane group and in 5% of the sevoflurane group. Induction with both anesthetics caused significant decreases from baseline blood pressure levels but no significant changes in heart rate. CONCLUSIONS: Inhaled sevoflurane in 60% nitrous oxide provides rapid but gentle anesthetic induction, with hemodynamic stability and a low incidence of airway complications. Sevoflurane is therefore a reasonable alternative to halothane for pediatric surgery.

Anesthesia, Inhalation↗
PubMed2005

Gas-phase positive ion chemistry of 1-bromo-1-chloro-2,2,2-trifluoroethane (halothane) upon electron ionization within an ion trap mass spectrometer.

The positive ion chemistry occurring within an ion trap mass spectrometer upon electron ionization of 1-bromo-1-chloro-2,2,2-trifluoroethane, the important anaesthetic halothane, has been mapped by means of collision-induced decomposition and ion/molecule self-reaction experiments. Ionized halothane (M+*) reacts with neutral halothane to form the ionized olefin [ClBrC=CF2]+*. via HF elimination. Among the ionic fragments, [M-Br]+ and [M-F]+ react with halothane via chloride abstraction while [M-Cl]+ is unreactive under the same experimental conditions. Substituted methyl cations CHFX+ and CF2X+ (X = F, Cl, Br) undergo halide transfer processes, their reactivity being highest for X = F. Ionized carbenes CXY+ (X,Y = F,F; H,Br; H,Cl; H,F) react with halothane to form CClXY+ and CBrXY+, whereas CF+ inserts into the C-Cl bond to form CF3+ and CClF2+. Finally, Br+ and Cl+ react with halothane by charge transfer. Collision-induced dissociation experiments disclosed interesting rearrangements involved in the dissociations of +CHX-CF3 ions (X = Br, Cl), which undergo fluorine migration and elimination of CF2, as already observed for +CCl2-CF3 in a previous investigation.

Journal Article↗
PubMed1991

Hypoxic ventilatory response in cats lightly anesthetized with ketamine: effects of halothane and sevoflurane in low concentrations.

The effect of low concentration sevoflurane and halothane on the ventilatory response to isocapnic hypoxia was studied in sixteen cats. The cats were divided into two groups, sevoflurane group and halothane group, of eight subjects each. As parameters of the hypoxic ventilatory response, A value [the slope of the hyperbolic curve, V(E) = V(0) + A/(Pa(O)(2)-32)] and ratio of V(50) (the minute volume obtained from the hyperbolic equation when Pa(O)(2) = 50 mmHg) to V(0) were studied. These two parameters were examined at three states, sedative state with ketamine as the control, ketamine plus 0.1 MAC inhalation anesthetic, and ketamine plus 0.5 MAC inhalation anesthetic. In the sevoflurane group, the A values were 4789 +/- 1518, 2187 +/- 1214, 1730 +/- 880 (mean +/- SE. ml.min(-1).mmHg) at the control state, 0.1 MAC and 0.5 MAC, respectively. In the halothane group, the A values were 6411 +/- 2368, 2529 +/- 842 and 2372 +/- 545, respectively. The ratios of V(50) to V(0) were 1.32 +/- 0.09, 1.22 +/- 0.09, 1.25 +/- 0.08 in the sevoflurane group, 1.47 +/- 0.18, 1.32 +/- 0.11, 1.54 +/- 0.18 in the halothane group, respectively. The A value at 0.1 MAC of the halothane group was less than the control value significantly. This proved that even low concentration halothane depressed the hypoxic ventilatory responses. The depression of hypoxic ventilatory response could cause postanesthetic hypoventilation. On the other hand, we could not find significant depression on the hypoxic ventilatory response in the sevoflurane group, but we should notice that variances of the hypoxic ventilatory response were large.

Journal Article↗
PubMed1993

Effects of halothane and isoflurane anesthesia on sympathetic adrenal nerve responses to carbon dioxide challenge in rats.

We studied the influence of two volatile anesthetics, halothane and isoflurane, on the circulatory and sympathetic nerve responses to carbon dioxide (9% CO2) in rats. Systolic blood pressure was depressed throughout the CO2 challenge and after an initial reduction, a gradual increase was observed in heart rate. Sympathetic adrenal nerve action potentials (SANA) significantly increased in contrast to negative responses in the circulatory functions. SANA responses against time were trapezoid in shape. There were no significant differences in SANA responses between 1% (1 MAC) and 1.5% (1.5 MAC) halothane groups, nor between 1.4% (1 MAC) and 2% (1.5 MAC) isoflurane groups. Halothane and isoflurane, therefore, did not produce dose-dependent effects on sympathetic response to hypercapnia within these concentrations. The maximum changes in SANA from the baseline values were 110% and 40% for the halothane and isoflurane groups, respectively. The sympathetic reflex response to hyperacapnia was retained at 1.5 MAC for both anesthetics, though isoflurane depressed these responses more markedly than halothane. Our results suggest that halothane is a more preferable anesthetic than isoflurane when viewed from the standpoint of preservation of sympathetic nerve response in such undesirable situations as severe hypercapnia occurring during anesthesia.

Journal Article↗
PubMed1989

Effects of halothane and hypoxia on hepatic oxygen metabolism in the dog.

Hepatic oxygen delivery and consumption were assessed in mongrel dogs receiving 2MAC of halothane combined with graded hypoxic hypoxemia (21-8% oxygen). Hepatic blood flow was measured using electromagnetic flowmetry; hepatic oxygen delivery and consumption were calculated from measured hepatic blood flow and oxygen content in hepatic arterial, portal venous and hepatic venous blood. In hypoxia-halothane group, total hepatic blood flow decreased at mild hypoxia (15% O2) from control value, but recovered to control level at moderate hypoxia (10% O2), then again decreased at 8% O2. Oxygen supply to the liver was decreased with the augmentation of hypoxia in hypoxia-halothane and hypoxia-alone groups, and it was significantly lower in the hypoxia-halothane group at 15 and 12% O2. Hepatic oxygen consumption also decreased from air control values with the increment of hypoxia, but there was no significant difference between the groups. Arterial ketone body ratio, which indicates mitochondrial energy charge level, decreased with the development of hypoxia but there was no significant difference in this ratio between the groups. These results show that halothane aggravated oxygen supply to the liver at mild to moderate hypoxia (15-12% O2), but did not worsen it specifically at more serious hypoxia (10-8% O2) compared with hypoxia alone. Hepatic hypoxia itself could not thus be a main cause of halothane hepatotoxicity.

Journal Article↗
PubMed2006

Effect of medetomidine on respiration and minimum alveolar concentration in halothane- and isoflurane-anesthetized dogs.

OBJECTIVE: To evaluate the effect of medetomidine on minimum alveolar concentration (MAC), respiratory rate, tidal volume, minute volume (V(M)), and maximum inspiratory occlusion pressure (IOCP(max)) in halothane- and isoflurane-anesthetized dogs. ANIMALS: 6 healthy adult dogs (3 males and 3 females). PROCEDURE: The MAC of both inhalants was determined before and 5, 30, and 60 minutes after administration of medetomidine (5 microg/kg, IV). Dogs were subsequently anesthetized by administration of halothane or isoflurane and administered saline (0.9% NaCl) solution IV or medetomidine (5 microg/kg, IV). Respiratory variables and IOCP(max) were measured at specific MAC values 15 minutes before and 5, 30, and 60 minutes after IV administration of medetomidine while dogs breathed 0% and 10% fractional inspired carbon dioxide (FICO2). Slopes of the lines for VM/FICO2 and IOCP(max)/FICO2 were then calculated. RESULTS: Administration of medetomidine decreased MAC of both inhalants. Slope of V(M)/FICO2 increased in dogs anesthetized with halothane after administration of medetomidine, compared with corresponding values in dogs anesthetized with isoflurane. Administration of medetomidine with a simultaneous decrease in inhalant concentration significantly increased the slope for V(M)/FICO2, compared with values after administration of saline solution in dogs anesthetized with halothane but not isoflurane. Values for IOCP(max) did not differ significantly between groups. CONCLUSIONS AND CLINICAL RELEVANCE: Equipotent doses of halothane and isoflurane have differing effects on respiration that are most likely attributable to differences in drug effects on central respiratory centers. Relatively low doses of medetomidine decrease the MAC of halothane and isoflurane in dogs.

Anesthetics, Inhalation↗
PubMed1963

Mechanism whereby halothane reverses the pressor responses to acetylcholine.

The initial and secondary components of the biphasic pressor response to acetylcholine in the atropinized dog were analysed separately. Deep halothane anaesthesia reversed the initial pressor response to acetylcholine owing to a decrease in total peripheral vascular resistance in the absence of an increase in cardiac output. The secondary pressor response was not reversed but was suppressed owing to a marked reduction of the increase in cardiac output responsible for this pressor response; total peripheral resistance increased. Conversely, halothane anaesthesia did not block the increase in blood glucose concentration resulting from the injection of acetylcholine. Thus, the change induced by halothane in the secondary pressor phase was apparently a consequence of cardiac depression rather than of adrenal medullary blockade. Compound P-286 (N-diethylaminoethyl-N-isopentyl-N'N'-di-isopropylurea), which produces a change in the pressor response to acetylcholine similar to that induced by halothane, prevents the hyperglycaemia due to acetylcholine. In some experiments, deep halothane anaesthesia depressed the cardiac inotropic but not the chronotropic response to acetylcholine. Such selective blocking action is believed to have a bearing on production of arrhythmias.

Acetylcholine↗
PubMed1998

Can a difference in chest wall mechanics explain the lower respiratory drive during propofol versus halothane anesthesia in children?

This article extends previous work which suggested that respiratory drive was lower during propofol compared with halothane anesthesia. The aim of this study was to assess simultaneously chest wall motion, measured with respiratory inductive plethysmography (RIP), and respiratory drive measured by P0.1 the pressure generated during the initial 100 msec of an occluded inspiratory effort. Ten healthy children age 3 to 6 years who presented for a dental restorative procedure that required in excess of 2.5 hours were recruited. Patients were anesthetized with propofol (2.5 mg x kg(-1); 15 mg x kg(-1) x hr) or halothane (1.25%), in a randomized crossover study design. Following induction of anesthesia, RIP bands were placed at the level of the nipples and the umbilicus for the measurement of rib cage and abdomen excursion, respectively. Flow and airway pressure were measured. A manually operated pneumatic balloon was used for brief airway occlusion. Following a 60-minute washin/out of the anesthetic, the children were removed from mechanical ventilation and spontaneous ventilation was reinstated. The RIP signals were calibrated by the method of simultaneous solution of equations. The phase lag was calculated. During airway occlusion the maximal excursion of the calibrated rib cage trace (RMAX) was measured; a negative value indicated retraction of the rib cage. Respiratory drive was assessed both at a fixed interval (100 msec) (P0.1) and fixed proportion (10%) (P10%) of the occluded inspiratory effort. Significance of differences were assessed with a paired t-test (P-value < 0.05). Thoracoabdominal asynchrony was greater during halothane than propofol anesthesia, as was the amount of rib cage retraction, evidenced by lower values of RMAX; respiratory drive was higher during halothane than propofol anesthesia, as evidenced by higher values of both P0.1, and P10%. We conclude that during halothane anesthesia altered chest wall mechanics may result in a greater respiratory drive than during propofol anesthesia.

Anesthesia, General↗
PubMed2005

In vivo interaction of pulmonary intravascular macrophages with activated platelets in microvessels of equine lung after multiple exposures to halothane, isoflurane, and thiamylal: a comparative ultrastructural and cytochemical study.

The pulmonary intravascular macrophages (PIMs) of equines contain a unique electron-dense surface coat that is predominantly composed of lipoproteins. A single exposure of inhalatory halothane causes mobilization of the surface coat into the endocytotic system of the PIMs, followed by expansion of the Golgi apparatus and its enrichment with acid phosphatase. Simultaneously, the cells of the lymphocytic series show hyperplasia in the form of mitotic changes inside the microvascular compartment of the lung. Halothane is known to cause acute and chronic hepatotoxicity because of its biotransformation into trifluoroacytelated polypeptides. The present study was designed to examine the comparative effects of reexposures of inhalatory doses of halothane, isoflurane, and the intravenous barbiturate thiamylal sodium in ponies to evoke a stronger response in the PIMs after four exposures at increasing intervals of 1, 2, and 6 weeks. Ultrastructural and cytochemical evidence is presented that halothane induced translocation of the surface coat into the vacuolar system of the PIMs, followed by expansion of the Golgi apparatus and its enrichment with acid phosphatase. The cell membrane was thrown into extraordinary lamellipodial extensions, which enabled the PIMs to interact with platelets within the narrow confines of the pulmonary capillaries. The relationship between PIMs and platelets developed into large platelet aggregates. Isoflurane and thiamylal sodium did not affect the circulating platelets, although the surface coat was translocated into the endolysosomes in both situations. Although isoflurane is a lipid-soluble inhalant anesthetic similar to halothane, it is subject to very little biotransformation after use and in the present model demonstrates no immune response.

Acid Phosphatase↗
PubMed1983

Local cerebral glucose consumption in the rat. I. Effects of halothane anesthesia.

Rates of cerebral glucose utilization were measured by means of the autoradiographic 2-deoxy-D-(1-14C)glucose technique in normal rats under light halothane-anesthesia. Three types of region-specific metabolic alterations were elicited by inhalation of 0.5% halothane. The most striking effect observed was a significant increase of glucose consumption within the locus coeruleus, substantia nigra compacta and reticulata, interpeduncular nucleus, hippocampus, and fornix of the anesthetized animals in comparison to the corresponding brain areas of the conscious control rats. Halothane-anesthesia was also associated with significant metabolic depression in 21 (out of the 74 examined) discrete regions of the rat brain, distributed within the pons, cerebellum, diencephalon, and cortex, and was more prevalent in thalamus and neocortex. However, halothane failed to alter consistently the rates of glucose utilization in the rest of the rat brain areas investigated. The present findings suggest that halothane specifically alters the regional cerebral glucose utilization, with some limbic system components and the basal ganglia displaying increased metabolism, in contrast to the sensorimotor system which demonstrates significantly decreased metabolic activity.

Anesthesia, General↗
PubMedDate not supplied

Leakage of mitochondrial and cytosolic GOT in isolated rat hepatocytes exposed to halothane: an immunohistochemical study.

The leakage of mitochondrial (m-) and cytosolic (s-) aspartate aminotransferases (glutamic-oxaloacetic transaminase: GOT) from isolated hepatocytes exposed to halothane was investigated immunohistochemically. In control isolated hepatocytes, a large number of cells were immunopositive (m-GOT, 85%; s-GOT, 98.5%) at various intensities. Reaction products of m-GOT-immunohistochemistry (m-GOT-I) were seen exclusively in mitochondria, while those of s-GOT (s-GOT-I) were seen in the cytoplasm. When treated with low concentrations of halothane (up to 0.75%), the number of strongly m-GOT-I-immunopositive cells was reduced to half, while that of s-GOT-I showed no noticeable change. The number of m-GOT-I-immunonegative cells showed a negligible increase, while that of s-GOT-I increased gradually. At higher concentrations of halothane (1% or more), strongly immunopositive cells in both m- and s-GOT-I almost disappeared, while immunonegative cell numbers predominantly increased. This study showed that the isolated hepatocyte system was not homogeneous with regard to the quantity of GOT isozymes, and that halothane could induce the leakage of these isozymes from hepatocytes, along with inducing ultrastructural abnormalities, even at the lowest concentration used (0.5%). Furthermore, the data appear to indicate that the sensitivity of isolated hepatocytes to halothane is dependent on the nature of the hepatocyte itself and on the nature of both types of GOT isozymes.

Animals↗
PubMedDate not supplied

In vivo 19F NMR studies of hyperthermia: hydrophobic environments probed by halothane.

The steady-state distribution of the general anesthetic halothane in different rat tissues, including a renal adenocarcinoma with and without hyperthermia treatment, has been evaluated by in vivo 19F NMR spectroscopy. The 19F spectra of halothane (which is a hydrophobic probe) from within tissue show differences in the partitioning between normal rat tissues and adenocarcinoma. Muscle, as a control tissue, exhibits a single large resonance around 0 ppm. However, the adenocarcinoma exhibits two slow-exchanging resonances separated by 0.3 ppm with the one at the more hydrophobic chemical shift being more sensitive to hyperthermia treatment. The results from this tumor model suggest that 19F NMR spectroscopy may be useful first in detecting a change in hydrophobic environments using a lipophilic probe such as halothane, and secondly in monitoring the effects of hyperthermia, a treatment whose effectiveness may involve changes at the level of the plasma membrane. Under conditions of continuous delivery, a resonance which is not detected in the spectra of halothane in excised tissue appears 5 ppm downfield from the resonance for halothane localized in tissues. A rotating frame experiment is used to show that this resonance is derived from anesthetic absorbed on the tissue surface.

Animals↗
PubMed1994

Halothane anesthesia enhances the effect of dopamine uptake inhibition on interstitial levels of striatal dopamine.

The anesthetic, isoflurane, has been shown to potentiate the ability of the dopamine (DA)-uptake inhibitor, nomifensine, to increase the brain interstitial dopamine level ([DA]e). Since the effect of the more commenly used anesthetic, halothane, on this system is unknown, we determined [DA]e by microdialysis in the striatum of rats, conscious or anesthetized with halothane, in the presence of the more selective DA uptake inhibitor, vanoxerine (GBR 12909), or the DA releaser, d-amphetamine. Basal [DA]e was not changed by halothane. However, in halothane-anesthetized rats, the vanoxerine (3 mg/kg i.v.)-induced DA response increased severalfold compared to the response in conscious rats. The initial peak response to d-amphetamine (1 mg/kg i.v.) did not change, but the late response (1-3 h after injection) was augmented in anesthetized rats. Halothane is believed to increase firing of DA neurons in the substantia nigra and, hence, to release striatal DA. We hypothesize that [DA]e is maintained at a normal level during the increased firing by equally increased activity of the DA transporter. However, when the DA transporter is blocked by vanoxerine, the increased DA release is unimpaired and [DA]e rises.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

Hepatic microsomal enzyme function in technicians and anesthesiologists exposed to halothane and nitrous oxide.

It is controversial whether daily occupational exposure to halothane stimulates (induces) the hepatic microsomal enzyme function in man. We investigated two groups of persons with different degrees of exposure to halothane: Six technicians who for years had been employed with repair and control of anesthesiologic equipment resulting in exposure to about 7 ppm of halothane and 50 ppm of nitrous oxide, and seven anesthesiologists exposed during months to about 2 ppm of halothane and 75 ppm of nitrous oxide. The clearance of antipyrine was determined from saliva concentrations before and 4 wk after discontinuation of exposure. Matched control persons were investigated simultaneously. No significant differences were found between the half-life, apparent volume of distribution, or clearance of antipyrine either within the groups or between the groups. If the antipyrine data from both exposure groups are compared to those of the control groups, the data exclude (95% confidence limit) that antipyrine metabolism increased by more than 3% during exposure to waste anesthetics. This indicates that occupational exposure to halothane in concentrations above the proposed maximal time weighted average concentration of 2 ppm does not change the microsomal activity.

Adult↗
PubMed1988

Differential effects of halothane on adult and juvenile sodium channels in human muscle.

Myoballs were cultured from biopsies of adult human skeletal muscle. Transient currents through the sodium channels were elicited by depolarizing a myoball membrane with the whole-cell patch-clamp technique. The properties of the sodium channels were determined from the Hodgkin-Huxley parameters (INa max, tau m, tau h, h infinity-curve) derived from these transients. Halothane, when applied at 3.4 mmol/l (approximately 15 kPa), blocked about 50% of the current through the adult, TTX-sensitive sodium channels but had little effect on the current through the juvenile, TTX-insensitive sodium channels. At greater than 12 mmol/l, halothane blocked both channel types completely. The time constants of activation and inactivation were decreased in the presence of 3.4 mmol/l halothane but not enough to account for the decrease of the current amplitude. Halothane shifted the h infinity-curves of both channel types toward more negative potentials by an amount that was roughly proportional to its concentration. Myoballs from a man susceptible to malignant hyperthermia (MH) gave the same results as the controls indicating that the halothane effect on the action potential of MH-susceptible muscle are not mediated by a specific effect on the sodium channels.

Action Potentials↗
PubMed1988

Influence of ventilatory and circulatory changes on the pharmacokinetics of halothane and isoflurane.

In two groups of dogs, uptake and elimination of halothane and isoflurane were studied using a closed-loop anesthesia system which automatically controlled end-tidal halothane or isoflurane partial pressure at minimal alveolar concentration (MAC) equivalent levels. Hemodynamic and respiratory variables were recorded and the anesthetic partial pressure was measured in the inspired and expired air, as well as in the arterial, cerebrovenous and mixed venous blood. Data were recorded during wash-in, hyperventilation, hypercirculation, hypotension and wash-out. For halothane, the controller delivered a higher inspired partial pressure than for isoflurane to compensate for the higher blood/gas partition coefficient. This was especially pronounced during the wash-in and the hypercirculation periods. Smaller differences between halothane and isoflurane partial pressures occurred during hyperventilation, hypotension and the wash-out period and could be explained by the lower solubility of isoflurane. These results show that even under unstable ventilatory and hemodynamic conditions, the inspired concentration of isoflurane has to be adjusted less often and to a smaller degree than that of halothane if end-tidal concentrations are to be maintained constant.

Animals↗
PubMed1989

Epidural morphine reduces halothane MAC in the dog.

Morphine, 0.1 mg.kg-1 was administered epidurally on two different occasions to ten dogs to determine the effect of two different volumes of saline dilution, 0.13 and 0.26 ml.kg-1, on the minimum alveolar concentration (MAC) of halothane as determined by subcutaneous electrical current applied to the fore and hind limbs in a random order. Following MAC determination with halothane alone, epidural morphine was administered and MAC was redetermined. Epidural morphine significantly reduced, P less than 0.001, the MAC of halothane for fore and hind legs in both volume groups; from 1.04 +/- 0.038 to 0.68 +/- 0.034 and 0.60 +/- 0.017 for for and hind limbs, respectively, in the large volume group, and from 0.96 +/- 0.038 to 0.66 +/- 0.088 and 0.60 +/- 0.030 for fore and hind limbs, respectively, in the small volume group. The reduction in MAC was significantly greater, P less than 0.025, in the hind limb. This study indicates that epidural morphine reduces the halothane requirements in the dog in a segmental manner. The volume of administration was not shown to be critical. Epidural morphine, 0.1 mg.kg-1, diluted in 0.13 to 0.26 ml.kg-1 saline produces significant analgesia in the dog as far forward as the fore limb and will reduce the halothane requirement to permit surgery.

Analgesia, Epidural↗
PubMed1990

Diltiazem and nifedipine reduce the in vitro contracture response to halothane in malignant hyperthermia-susceptible muscle.

The effects of diltiazem (1 microM) and nifedipine (1 microM) were examined separately on the in vitro halothane tests for malignant hyperthermia (MH) susceptibility. Eighteen patients with MH susceptibility were diagnosed as MH-susceptible (MHS) according to the protocol of the European MH Group. In addition, halothane tests were carried out in the presence of either diltiazem (ten patients) or nifedipine (eight patients). These two calcium channel blockers significantly reduced the halothane contracture. Furthermore, in five of the ten MHS patients tested in the presence of diltiazem as well as in five of the eight MHS patients tested in the presence of nifedipine the halothane contracture test could be classified as negative. It is concluded that the presence of clinical concentrations of either diltiazem or nifedipine in the muscle bath affects the in vitro discrimination for MH susceptibility to halothane.

Depression, Chemical↗