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[Comparative study of the behavior of isoflurane and halothane in pediatric anesthesia].

This study involves 60 patients below the age of 14 years who were subjected to short duration surgical procedures under inhalation anesthesia with halothane and isoflurane at equivalent CAM in 50% protoxide. The objectives of the study were: a) to establish which of the two inhalational agents produced the more rapid anesthetic induction; b) to determine which exerted the more marked potentiation of the neuromuscular blockade induced by succinylcholine, and c) to compare the anesthetic quality during the induction and recovery periods of both halogenated agents. Induction was more rapid after halothane (mean induction time of 2.91 +/- 0.97 min) than after isoflurane (mean induction time of 6.24 +/- 2.88 min; p less than 0.001). Potentiation of succinylcholine induced neuromuscular blockade was greater after isoflurane than after halothane: the mean time of apnea was 4.56 +/- 1.82 min for isoflurane and 3.41 +/- 1.63 min for halothane (p less than 0.05). Undesirable effects were larger in patients treated with isoflurane than in patients anesthetized with halothane (mean score: 12.60 +/- 3.53 points vs 14.41 +/- 2.33 points; p less than 0.001). The analysis of anesthetic quality during the recovery period gave a mean punctuation of 16.62 +/- 2.21 to patients treated with halothane, whereas patients anesthetized with isoflurane showed a lower score of 14.25 +/- 1.99 points (p less than 0.001). The higher scores corresponded to the most well tolerated anesthetic induction and recovery. The highest attainable score in this study was 18.

Adolescent↗
PubMed1992

Halothane relaxes previously constricted human epicardial coronary artery segments more than isoflurane.

To compare the vasodilatory effects of isoflurane versus halothane on coronary arteries in vitro, we studied the capacity of isoflurane and halothane to relax resting and previously constricted human coronary artery segments with use of in vitro tension recording. Human epicardial coronary artery segments (1.5-2.0 mm outside diameter) were obtained from hearts excised from recipient patients at time of heart transplantation. The effects of 0.5%, 1.0%, 2.0%, and 3.0% isoflurane or halothane on resting coronary artery segments stretched to their optimal resting tension were determined. Next, after removal of anesthetic from the bathing solution, the segments were constricted with K+ (60 mM), and this contraction was allowed to plateau. The arteries were then again exposed to isoflurane or halothane at 0.5%, 1.0%, 2.0%, and 3.0% concentrations. Isoflurane and halothane had no effect on noncontracted coronary artery segments stretched to their optimal resting tension. Halothane caused significant relaxation of K(+)-induced (60 mM) contractions at 2.0% and 3.0% but not at lower concentrations. Isoflurane did not cause significant relaxation of K(+)-induced (60 mM) contractions at any concentration studied. Our studies indicate that under the conditions studied, isoflurane at clinically relevant concentrations is not a significant coronary dilator.

Coronary Vessels↗
PubMed1992

Halothane 2% for caesarean section.

During the induction-delivery interval for Caesarean section delivery, 2% halothane in pure oxygen was administered. The technique was compared to a 0.5% halothane in 50% oxygen/50% nitrous oxide anaesthesia. When a continuous infusion of oxytocin was administered, no excessive haemorrhage was seen. No maternal reminiscence was seen using 2% halothane, but awareness was recorded using 0.5% halothane in 50% nitrous oxide in 15% of the mothers. When there were no signs of preoperative fetal distress, the neonates were unaffected by the halothane concentration provided the induction-delivery interval was short. In cases of fetal distress, the administration of 2% halothane further aggravated the condition of the neonates, as indicated by lowered 1-min Apgar scores, umbilical oxygen tensions, pH and base excess values.

Adult↗
PubMed1991

Aerobic dehalogenation of halothane showing different substrate dependency from anaerobic dehalogenation in liver microsomes of guinea pig.

The formation of trifluoroacetic acid (TFAA) from halothane under aerobic conditions and that of chlorotrifluoroethane (CTE) and chlorodifluoroethylene (CDE) from halothane under anaerobic conditions were studied using guinea pig liver microsomes. The formation of TFAA was inhibited by specific inhibitors of cytochrome P450 (P450), such as carbon monoxide and metyrapone and was dependent upon P450 contents. The maximum activity of the TFAA formation was obtained at pH 6.0. On the other hand, the maximum activity to form CTE and CDE was obtained at pH 7.4. The formation of TFAA reached a plateau at a halothane concentration above 0.17 mM, but the rate of formation of CDE and CTE was dependent upon a halothane concentration up to 1.5 mM. The values of apparent Michaelis-Menten constant (Km) and maximum velocity (Vmax) for TFAA formation were 0.067 mM and 0.349 nmol/nmol P450/min respectively, those for CDE formation were 0.983 mM and 0.326 nmol/nmol P450/min respectively, and those for CTE formation were 1.71 mM and 0.752 nmol/nmol P450/min respectively. These results showed clearly that the formation of TFAA, CDE and CTE was catalyzed by the P450 system in guinea pig liver microsomes. Under optimal conditions, saturation was observed in the formation of TFAA from halothane at a halothane concentration above 0.17 mM but the formation of CDE and CTE was not saturated at this concentration, and the value of apparent Km for TFAA formation was lower than those for CDE and CTE formation.

Aerobiosis↗
PubMed1991

Comparison of inhalation induction with isoflurane or halothane in children.

Thirty-six children (mean age 2.4 years) premedicated with oral chloral hydrate 70 mg kg-1 and atropine 0.03 mg kg-1 were anaesthetized with either 3.75% isoflurane or 2.5% halothane in 70% nitrous oxide in oxygen. The eyelash reflex disappeared in 39 +/- 7 s (mean +/- SD) with isoflurane and in 56 +/- 16 s with halothane (P less than 0.001). Tachypnoea was seen with both anaesthetics. Coughing, breath holding, stridorous breathing and respiratory depression were seen during isoflurane but not during halothane induction (P less than 0.01). In nine of 20 children anaesthetized with isoflurane, the ventilation had to be assisted before intubation. Endotracheal intubation was possible in 224 +/- 35 s with isoflurane and in 281 +/- 64 s with halothane (P less than 0.01). Intubating conditions were satisfactory in 80% of the children anaesthetized with either volatile agent. Cardiovascular responses to endotracheal intubation were minimal with both anaesthetics. No cardiac dysrhythmias were noted. Heart rate was higher during isoflurane than during halothane induction. Diastolic arterial pressure was lower during isoflurane than during halothane induction immediately and 5 min after intubation.

Analysis of Variance↗
PubMed1991

[Effects of halothane on spinal dorsal horn WDR(wide dynamic range) neuronal activity in cats].

The effects of halothane (0.2%, 0.5%, and 1.0%) on the spinal dorsal horn wide dynamic range (WDR) neuronal activity was studied in either spinal cord intact or spinal transected cats. Extracellular activity was recorded in the dorsal horn from single WDR neurons responding to noxious and non-noxious stimuli applied to the cutaneous receptive fields on the left hind foot pads of intact or decerebrate, spinal cord transected (L 1-2) cats. When 10 micrograms of bradykinin was injected into the femoral artery ipsilateral to the recording site as the noxious test stimulus in the spinal cat, all of 7 WDR neurons gave excitatory responses which were not depressed by 0.2% and 0.5% halothane but were depressed significantly by 1.0%. On the other hand, when the injection of 10 micrograms of bradykinin into the femoral artery ipsilateral to the recording site was used in the intact cat, 7 of 14 WDR neurons (50%) gave excitatory responses, which were not depressed by 0.2% halothane but were significantly depressed by 0.5% and 1.0% halothane, and 7 of 14 WDR neurons (50%) gave inhibitory responses, which were significantly depressed by 0.2%, 0.5%, and 1.0% halothane. We have found that halothane reduces the excitation as well as the inhibition of dorsal horn WDR neuronal activity induced by bradykinin injection.

Animals↗
PubMed1990

pH-dependent interaction of halothane upon thiopental binding to human serum albumin.

At pH 7.4 the binding of thiopental to human serum albumin (HSA) was increased in the presence of halothane. In order to obtain information about the mechanism of this interaction, in vitro binding experiments by means of equilibrium dialysis were carried out at different pH values. At pH 4.97 the binding of thiopental to HSA 1% was low (23% bound) and not influenced by halothane. An increase of thiopental binding caused by halothane could be seen at pH 7.4 (55% bound vs. 41% in the control = without halothane) and at pH 8.23 (62% vs. 54%). At pH 10.15 an opposite interaction was found: in the presence of halothane thiopental binding was considerably decreased (36.2% vs. 47.0% in the control). Evaluation of the binding parameters of experiments using increasing substrate concentrations (Scatchard plot) revealed quite different changes of the two classes of binding sites of HSA for thiopental. It is assumed that halothane causes reversible conformational changes of the albumin molecule resulting in altered binding characteristics for thiopental.

Binding Sites↗
PubMed1990

[Ventilatory effects of halothane and enflurane in dogs].

The ventilatory effects of halothane and enflurane were studied in permanently tracheostomized dogs at the same anesthetic depth of 1 MAC. Inspiratory and expiratory durations were longer and tidal volume greater during enflurane than during halothane anesthesia. Mean inspiratory flow rate and minute ventilation during enflurane anesthesia were less than those during halothane anesthesia. As a result, end-expiratory carbon-dioxide concentration was higher during enflurane than during halothane anesthesia. When end-expiratory carbon-dioxide concentration was held at 7.5%, tidal volume was not different between the two anesthetics, while the difference of other parameters still remained. In addition, the magnitude of Hering-Breuer reflex determined by end-expiratory airway occlusion was essentially identical between halothane and enflurane anesthesia. The present results indicate that 1) depressant effect of enflurane on respiratory drive is greater than that of halothane and 2) the two anesthetics act on the respiratory timing mechanism differently.

Animals↗
PubMed1990

[Interaction of halothane and PGE1 on ICG excretion].

We performed ICG-test during surgery to study the effect of halothane on ICG excretion in humans. We also evaluated the effect of PGE1 on ICG excretion concomitantly used during halothane anesthesia. A significant decrease in ICG clearance occurred in the patients who received only halothane to reduce the systolic arterial pressure (SAP) to 70% of the preoperative value. The reduction in SAP induced by PGE1 together with halothane, however, did not decrease the ICG clearance rate. We conclude that halothane may decrease the hepatic blood flow, but PGE1 may neutralize the effect of halothane, and maintain the hepatic blood flow in man.

Adult↗
PubMed1989

Effects of clinically effective concentrations of halothane on adrenergic and cholinergic synapses in rat brain in vitro.

The effects of clinically relevant concentrations of halothane on various synaptic events in rat brain were examined in vitro. Slices or membranes prepared from various brain regions were equilibrated with 1.25% halothane at 37 degrees C, resulting in tissue concentrations greater than those found in brains of completely anesthetized animals (greater than 40 nmol/mg of lipid). Under these conditions, no effects of halothane were observed on agonist or antagonist binding to alpha-1 adrenergic, beta adrenergic, alpha-2 adrenergic or muscarinic cholinergic receptors, or on the ability of 5'-guanylylimidodiphosphate to reduce agonist binding affinity. This concentration of halothane also had no effect on norepinephrine-stimulated cyclic AMP accumulation, or inositol phosphate accumulation in response to norepinephrine, carbachol, histamine or 5-hydroxytryptamine. Halothane did reduce potassium-evoked release of [3H]norepinephrine from slices of rat cerebral cortex although it did not affect potassium-evoked release of [3H]acetylcholine. These results suggest that halothane may be relatively specific in its synaptic actions and may affect depolarization-evoked release of norepinephrine at concentrations achieved clinically.

Acetylcholine↗
PubMed1989

Action of the stereoisomers of medetomidine, in halothane-anesthetized dogs.

This study was designed to investigate the anesthetic-reducing and cardiovascular effects of the stereoisomers of medetomidine in halothane-anesthetized male beagles. Anesthesia was induced by mask inhalation of halothane in oxygen, followed by 2h equilibration period. The minimum alveolar anesthetic concentration of halothane which prevented the animals from moving in response to a painful stimulus (MAC of halothane) was determined and baseline hemodynamic function was assessed. Dl-Medetomidine, at 3 doses (1, 3 and 10 micrograms.kg-1) was administered via the right atrial port over 15 minutes while maintaining the dog at its individual MAC for halothane. Ten minutes later, hemodynamic parameters were reassessed. MAC determination was then repeated. In two separate sets of experiments, dogs (n = 5 each) were administered either the d- or the 1-enantiomer of medetomidine and the same procedure followed as described above. MAC for halothane significantly decreased following dl-medetomidine administration in a dose-dependent fashion. The d-isomer displayed similar MAC-reducing effects while the 1-isomer was without effect. Neither isomer changed the mean arterial pressure while only and d-isomer significantly decreased heart rate and cardiac output.

Adjuvants, Anesthesia↗
PubMed1989

[The effects of halothane and epidural anesthesia on the gastric intramural pH and the pH of gastric juice].

To evaluate the effects of gastric intramural pH on intraluminal fluid of stomach during halothane anesthesia, the pH of gastric content and the gastric intramural pH measured by noninvasive method under halothane anesthesia were compared with those during epidural anesthesia. Nineteen patients without gastrointestinal disorders who received elective surgery were studied; 14 patients were anesthetized with N2O-O2-halothane and 15 patients were anesthetized with N2O-O2, flunitrazepam and lumber epidural anesthesia. The intramural pH was calculated from the Henderson-Hasselbalch's equation: intramural pH = 6.1 + ([HCO3-]/PCO2 X 0.0307), substituting [HCO3-] in arterial blood for [HCO3-] in tissue and PCO2 in gastric content for PCO2 in tissue. The pH of gastric content was elevated gradually under halothane anesthesia, but it was unchanged under epidural anesthesia. On the other hand the intramural pH was unchanged during both anesthetic methods and there were no significant differences between the two groups. These results suggest that the elevation of the pH of gastric content under halothane anesthesia is not the result of intragastric microcirculatory impairment and halothane may have other suppressive actions on gastric acid secretion.

Adult↗
PubMed1989

Porcine malignant hyperthermia susceptibility: halothane-induced increase in cytoplasmic free calcium in lymphocytes.

We tested the hypothesis that lymphocytes from swine with susceptibility to malignant hyperthermia (MH) had increased sensitivity to the membrane-perturbing effects of halothane that increase cytoplasmic calcium. Cytoplasmic concentration of ionized calcium in lymphocytes isolated from blood was determined in the presence and absence of halothane for 10 Pietrain x Poland China swine that were susceptible to MH and 20 Yorkshire swine that were resistant to MH. Calcium was determined by dual-emission spectrofluorometry and by measuring the ratio of free to calcium-bound form of the fluorescent calcium dye Indo-1. Mean values for calcium concentrations in lymphocytes from MH-susceptible (MHS) swine were 80% less than control values (40.5 +/- 38.8 and 185.3 +/- 91.6 nmol/L; P less than 0.01). Untreated lymphocytes from MHS swine accumulated calcium at half the rate observed for controls. Exposure to 1 mmol/L halothane resulted in a 3-fold increase of free calcium concentration to 127.9 +/- 81.3 nmol/L in the lymphocytes of MHS swine, but had no significant effect on lymphocytes from control swine (225.0 +/- 91.4; P less than 0.01). Exposure to 2 mmol/L halothane resulted in a 6-fold increase of free calcium concentration to 255.9 +/- 91.4 nmol/L in lymphocytes from MHS swine and a 63% increase in lymphocytes from controls (303.8 +/- 116). The rate of halothane-induced increase in cytosolic calcium was 13 times greater in lymphocytes from MHS swine, compared with controls. These data indicated that the molecular defect that results in halothane-hypersensitivity and is characteristic of muscle of MHS swine also occurs in lymphocytes from MHS swine.

Animals↗
PubMed1988

Global and regional myocardial blood flow and metabolism during equipotent halothane and isoflurane anesthesia in patients with coronary artery disease.

Global and regional myocardial blood flow and metabolism were examined in 20 patients with coronary artery disease before surgical stimulation. Half were anesthetized with halothane (0.8%) and half with isoflurane (1.2%). Coronary perfusion pressure decreased similarly in both groups. During halothane anesthesia coronary sinus blood flow, an index of global perfusion, decreased from an awake value of 129 +/- 7 to 97 +/- 7 ml/min (P less than 0.05), and great cardiac vein blood flow, an index of regional perfusion, decreased from 60 +/- 8 to 44 +/- 5 ml/min (P less than 0.05). In contrast, during isoflurane anesthesia global coronary blood flow increased from 131 +/- 13 to 153 +/- 16 ml/min (P less than 0.05), while regional blood flow decreased from 68 +/- 7 to 56 +/- 6 ml/min (P less than 0.05). Thus, the ratio of great cardiac vein blood flow to coronary sinus blood flow was unchanged during halothane anesthesia but decreased significantly during isoflurane. Neither global nor regional coronary vascular resistance was altered by halothane, whereas isoflurane decreased global coronary vascular resistance without affecting regional coronary vascular resistance. All patients receiving halothane had net myocardial lactate extraction. In the isoflurane group, four patients showed global lactate production and three regional lactate production. All patients demonstrating lactate production also developed electrocardiographic evidence of myocardial ischemia, which was not present before induction. The authors conclude that halothane is a preferable anesthetic to isoflurane in patients with coronary artery disease because the latter has the propensity to induce maldistribution of the coronary circulation and myocardial ischemia.

Adult↗
PubMed1987

Isoflurane has a greater margin of safety than halothane in swine with and without major surgery or critical coronary stenosis.

The fatal/anesthetic ratio (FAR) in 44 swine weighing 32.6 +/- 0.7 kg (SEM) was determined. Fatal anesthetic concentration (the numerator for FAR) was defined as the end-tidal concentration at which the pig lived at least 10 min, during experiments that involved step increments in anesthetic concentrations. Previously reported MAC was used as the "anesthetic" concentration (denominator) to determine FAR. Halothane was compared to isoflurane and the question of whether major surgery might reduce FAR was investigated. The major surgery groups included one open chest group with each volatile anesthetic studied during coronary reserve measurements, and two groups that had LAD critical coronary stenoses. Thus volatile agents were compared with vs without major surgery, and with vs without a critical coronary stenosis. The FAR for isoflurane was approximately double that of halothane. Further, addition of major surgery did not produce significant deterioration in FAR with isoflurane. In contrast, with halothane there was a significant (approximately 20%) decrease in FAR, despite values already only half that seen with isoflurane, when major surgery was added. Presence of a critical coronary stenosis was not associated with a worsened FAR for isoflurane or halothane. It was concluded that the fatal/anesthetic ratio for isoflurane in pigs is 1.9 times greater than that for halothane. Addition of major surgery did not affect FAR when isoflurane was the anesthetic but did when halothane was used. Critical coronary stenosis did not worsen FAR. Because these results are nearly identical with those reported previously in small mammals, the doubled safety margin seen with isoflurane may have clinical relevance.

Animals↗
PubMed1987

The effect of nitrous oxide on cortical cerebral blood flow during anesthesia with halothane and isoflurane, with and without morphine, in the rabbit.

The effect of nitrous oxide on cortical cerebral blood flow (CBF) was examined during a varying background anesthetic state in the New Zealand White rabbit. Seventy percent nitrous oxide resulted in significant and similar increases in CBF during anesthesia with both 0.5 MAC of halothane (44 +/- 14 to 63 +/- 17 ml.100 g-1.min-1) (mean +/- SD) and anesthesia with isoflurane (34 +/- 9 to 41 +/- 11 ml.100 g-1.min-1). During anesthesia with 1.0 MAC halothane or isoflurane, N2O also increased CBF, but the increments (halothane, 73 +/- 34 to 111 +/- 54 ml.100 g-1 min-1; isoflurane 34 +/- 13 to 69 +/- 34 ml.100 g-1.min-1) were significantly greater than those observed at 0.5 MAC. When 0.5 MAC halothane or isoflurane was supplemented with morphine (10 mg/kg followed by an infusion of 2 mg.kg-1.min-1), the CBF effect of N2O was not significantly different from that observed with 0.5 MAC alone. It was concluded that, in the rabbit, the effects of N2O on cortical CBF vary with the background anesthetic state and that the increase in CBF caused by N2O becomes greater as the end-tidal concentration of halothane or isoflurane increases from 0.5 to 1.0 MAC. Morphine, when added to 0.5 MAC of halothane or isoflurane, does not alter the effect of 70% N2O on cortical CBF.

Animals↗
PubMed1986

[Does halothane, in subnarcotic dosage, have a detectable broncholytic effect?].

The reaction of halothane in subnarcotic dosage (0.25-0.5 Vol.-%) e.g. with the cooperative patient, was tested at 32 patients with chronic obstructive pulmonary affection (from them 26 patients with pathological increased resistance of the respiratory system) concerning bronchial obstruction. The significant decrease of the respiratory rate and of the resistance of the respiratory system as well as the significant increase of the volume of the breath inspiration unambiguously prove, beside the influence on the subjective health and on the auscultatory findings, a bronchial-enlarging effect of halothane. At 10 patients with serious acute bronchial obstruction, which could not be cured by means of conventional medicamentous therapy, halothane was employed in subnarcotic dosage. In spite of the difficulties in the assessment of the halothane effect by pretreatment we relate the impressive, subjective and objective improvement in these patients to its bronchospasmolytic effect because of the immediate temporal association with the halothane inhalation. In case that there are missing contraindications and an insufficient effect of the conventional medicamentous therapy the use of halothane in subnarcotic dosage with acute serious bronchial obstruction is indicated.

Airway Resistance↗
PubMed1986

Effects of halothane and decreased PO2 on high energy phosphate levels maintained by isolated rat liver mitochondria.

Steady states of oxidative phosphorylation were achieved in mitochondrial suspensions continuously equilibrated with constant gas mixtures, simulating the conditions under which mitochondria contribute to the cellular energy status in vivo. The dependence of the mitochondria-maintained adenosine triphosphate/adenosine diphosphate (ATP/ADP) ratio on oxygen and halothane levels was examined at predetermined, clinically relevant concentrations of both gases. Inclusion of 1% halothane in the gas mixture decreased ATP/ADP by about half when mitochondrial respiration was supported by NAD-linked substrate (glutamate); succinate-supported ATP/ADP was not inhibited. With either substrate, and whether or not 1% halothane was present. ATP/ADP was unaffected by decreases in PO2 to values as low as 1.6 mm Hg. Under a range of typical in vivo conditions, therefore, 1% halothane significantly inhibited the mitochondrial contribution to steady state energy balance, whereas decreases in PO2 did not. Combined effects of 1% halothane and reduced PO2 on ATP/ADP were not seen, i.e., halothane did not increase the critical PO2 level (hypoxic threshold) for inhibition of mitochondrial ATP production.

Adenosine Diphosphate↗