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PubMed1988

[Autoregulation of the papillary vessels and their behavior as affected by halothane].

Halothane lowers the peripheral vascular resistance and blocks autoregulation in the cerebral vessels. Proceeding from the assumption that the papillary vessels behave in like manner, the authors examined increases in papillary pallor under artificial IOP elevation in anesthetized patients with and without Halothane, using the photopapillometer. This provocation test was conducted in 14 patients, first on one eye under normal (N2O/O2) anesthesia, then on the fellow eye after steady state had been attained with subsequently administered Halothane. By quantifying ocular circulatory conditions, the demonstration of the lowering of peripheral vascular resistance in the papillary vessels under Halothane was convincing; the blockage of autoregulation was less obvious. To explain these results the authors suggest that the two effects are gradual and mutually influential.

Adult↗
PubMed1981

[Halothane hazards for the team in the operation theatre (author's transl)].

Reports on undesirable side effects of halothane in patients undergoing anaesthesia and in persons with long-term exposure in the operation theatre require establishment of safe upper limits and of methods for monitoring. The main metabolite trifluoroacetic acid is most suitable for biological monitoring. During systematic exposure with graded halothane concentrations (8, 24 and 50 ppm, 6 hours daily, 5 days weekly, for one and two weeks) trifluoroacetic acid concentrations in blood and urine were determined regularly. It was shown that for biologic monitoring estimation in blood is clearly preferential to estimation in urine because of a narrower scatter. At the end of one week of exposure a steady state concentration is found in blood. There is a linear relation between its height and the inhalation concentration of halothane. A trifluoroacetic acid concentration of 2.5 micrograms/ml is considered as a risk-free value. This corresponds to a maximal theatre air concentration of 5 ppm halothane.

Halothane↗
PubMed1994

Genetic differences affecting the potency of stereoisomers of halothane.

The mechanism of action of volatile anesthetics is the subject of some debate. Much of the controversy has centered on whether the site of such actions is purely lipid in nature or may contain a protein target. This report studies the interaction of stereoisomers of halothane on the wild type and on a variety of genetic mutants of Caenorhabditis elegans. The mutants studied have previously been shown to have altered sensitivities to volatile anesthetics. In one mutant, fc34, (R)-halothane [the (+) isomer] was 3 times more potent than its S (-) isomer. Other mutants and wild-type animals displayed more modest differences in sensitivity to the enantiomers. The results indicate that a genetic pathway exists in C. elegans controlling sensitivity to halothane and that both lipid and protein targets may mediate halothane's effects.

Animals↗
PubMed2000

Binding of the general anesthetics propofol and halothane to human serum albumin. High resolution crystal structures.

Human serum albumin (HSA) is one of the most abundant proteins in the circulatory system and plays a key role in the transport of fatty acids, metabolites, and drugs. For many drugs, binding to serum albumin is a critical determinant of their distribution and pharmacokinetics; however, there have as yet been no high resolution crystal structures published of drug-albumin complexes. Here we describe high resolution crystal structures of HSA with two of the most widely used general anesthetics, propofol and halothane. In addition, we describe a crystal structure of HSA complexed with both halothane and the fatty acid, myristate. We show that the intravenous anesthetic propofol binds at two discrete sites on HSA in preformed pockets that have been shown to accommodate fatty acids. Similarly we show that the inhalational agent halothane binds (at concentrations in the pharmacologically relevant range) at three sites that are also fatty acid binding loci. At much higher halothane concentrations, we have identified additional sites that are occupied. All of the higher affinity anesthetic binding sites are amphiphilic in nature, with both polar and apolar parts, and anesthetic binding causes only minor changes in local structure.

Anesthetics, General↗
PubMed2005

Halothane, an effective infrequently used drug, in the treatment of pediatric status asthmaticus: a case report.

Asthma is the most common chronic disease of childhood. Despite a better understanding of the disease process and its management, status asthmaticus continues to be a life-threatening event. The use of volatile inhaled anesthetics is infrequently reported as adjunctive therapy to conventional treatment of this condition. We report the use of halothane in a mechanically ventilated pediatric patient with life-threatening status asthmaticus who was admitted to the pediatric intensive care unit (PICU) after failing to respond to standard medical therapy and noninvasive positive pressure ventilation. A 12-year-old African American male was seen in the emergency department and treated with intravenous corticosteroids, beta-agonist therapy. He deteriorated rapidly and required endotracheal intubation and mechanical ventilation. Two hours later, the patient developed an acute, severe respiratory acidosis (pH=6.97, PaCO2=171, PaO2=162, BE=1.7). Halothane was started at 2% by using the Siemens Servo 900C anesthesia ventilator. Improvement in both arterial blood gases and exhaled tidal volume were noted 30 minutes after initiation of the anesthetic gas. The patient remained on halothane for a total of 36 hours. No adverse effects associated with the use of halothane were noted. The patient was extubated to BiPAP 16/6, FiO2=0.30 at 68 hours and was discharged home 5 days later.

Acidosis, Respiratory↗
PubMed1977

Halothane in tissue of rats following repeated subanesthetic exposures.

Halothane in tissues of the rat has been measured as a function of time after five successive 3 hr exposures to 670 ppm halothane. In epididymal and perirenal fat, halothane concentrations diminished rapidly from 310 ppm to 1-2 ppm in 24 hr, with trace amounts detectable 5 days later. Brain and liver levels were reduced from 16 and 9 ppm to less than 1 ppm within 3 hr. Blood halothane was reduced from 3 ppm to less than 0.5 ppm in the same time.

Adipose Tissue↗
PubMed1976

The suppressive effect of halothane on DNA synthesis of immunocytes.

Mice, previously immunized with sheep erythrocytes, were anaesthetized with halothane and the splenic lymphoid cells were incubated with 3H-thymidine at 1-h intervals. Abiphasic response was observed; 0.9 and 1.5% halothane reduced 3H-thymidine incorporation into the primed lymphoid cells by 83 and 94% respectively, while 0.4% halothane stimulated it by 5% of control at 3H. Immunosuppression by halothane may be the result of reduced 3H-thymidine uptake of the dividing immunocytes.

Animals↗
PubMed1976

Lack of beta-adrenergic activity of isoflurane in the dog: a comparison of circulatory effects of halothane and isoflurane after propranolol administration.

The studies were undertaken to determine whether isoflurance inhalation is associated with a degree of beta-adrenergic action that is potentially important in clinical situations, and to compare the circulatory tolerance to isoflurane and halothane in dogs following beta blockade. We measured arterial and pulmonary artery pressure, left and right ventricular filling pressure, heart rate and cardiac output, and derived stroke volume and systemic and pulmonary vascular resistances in 13 mongrel dogs. The haemodynamic response to 1 MAC and 2 MAC isoflurane was studied in seven dogs and was similar before and after propranolol 0.1mg/kg i.v. In six dogs, propranolol 0.5mg/kg caused no significant changes in the circulatory response to 1 MAC and 2 MAC isoflurane or 1 MAC halothane. However, in three dogs, administration of 2 MAC halothane after propranolol 0.5mg/kg resulted in such profound circulatory depression as to preclude further study. These data suggest that (a) isoflurane possesses no clinically important beta-adrenergic stimulating activity; (b) there is no adverse drug interaction upon the circulation with the combination of isoflurane and propranolol; (c) in the presence of moderated profound beta-adrenergic blockade, 2 MAC isoflurane may be tolerated better than 2 MAC halothane.

Adrenergic beta-Agonists↗
PubMed1976

Haemodynamic interactions of high-dose propranolol pretreatment and anaesthesia in the dog. II: The effects of acute arterial hypoxaemia at increasing depths of halothane anaesthesia.

Beta-adrenergic blockade may impair the normal cardiovascular response to hypoxia occurring during general anaesthesia. The haemodynamic effects of acute hypoxia, induced by a 90-s period of ventilation with nitrogen, were studied during increasing depths of halothane anaesthesia up to a maximum of 2.5% inspired halothane in dogs chronically implanted with intracardiac catheters, a left-ventricular pressure transducer and an aortic blood flow transducer. An untreated group of dogs and a group which had been treated for 3 weeks with propranolol 20 mg/kg/day were compared. The beta-blocked group had lesser cardiac output values, left-ventricular contractility indices, external left-ventricular work and peak left-ventricular power at all depths of anaesthesia except 2.5% halothane, but both groups responded to hypoxia similarly at each depth of anaesthesia. Cardiac performance was enhanced in both groups during acute hypoxia. No adverse haemodynamic effect of the combination of propranolol, halothane and hypoxia was demonstrated.

Anesthesia, General↗
PubMed1977

Depression of hypoxic ventilatory response by halothane, enflurane and isoflurane in dogs.

The ventilatory responses to isocapnic hypoxia and hypercapnia were studied in six dogs each with a tracheostomy, awake and during anaesthesia with halothane, enflurane and isoflurane (1-2.5 MAC). Isocapnic hypoxic ventilatory response (HVR) was expressed as the parameter A, such that the greater the value of A, the greater the hypoxic response. In the anaesthetized dogs HVR (A) was reduced significantly from the awake value of 2010 +/- 172 (mean + SEM) to 630 +/- 173 by 1 MAC halothane, 495 +/- 105 by 1 MAC enflurane and 952 +/- 157 by 1 MAC isoflurane (PL0.05). All three anaesthetic agents produced significant depression of HUR at 1 MAC, but enflurane was more depressant than isoflurane. At 1.5 MAC all three anaesthetics produced equal and significant depression of HVR at equianalgesic concentrations. Further increases in anaesthetic concentration caused no increase in depression. Hypercapnic drive, as measured by the slope of the VE/PACO2 response curve, was reduced significantly from 9.75 litre min-1 kPa-1 +/- 2.4 in awake dogs to 0.83 +/- 0.56 after 1 MAC halothane, 0.68 +/- 0.53 after 1 MAC enflurane and 1.58 +/- 0.75 after 1 MAC isoflurane. In addition, hypercapnia-induced augmentation of the hypoxic drive was abolished by 1 MAC halothane or enflurane and diminished markedly by 1 MAC isoflurane. It may be clinically significant that hypoxia and hypercapnia during anaesthesia with these agents did not produce optimal stimulation of ventilation.

Anesthesia↗
PubMed1977

Halothane solubility in human blood.

In a study of the influence of nutritional state on halothane anaesthesia, results were obtained which showed how the blood/gas partition coefficient for halothane varied with blood chemistry in 20 patients undergoing elective surgery. For each patient the partition coefficient lambda was measured by equilibration at 37 degrees C of a blood sample with a 1% halothane in 5% carbon dioxide in air mixture, followed by chemical extraction and estimation of the halothane content by gas chromatography. The haematocrit and haemoglobin, serum albumin, total protein, triglyceride and cholesterol concentrations were measured by routine laboratory methods. Regressions were sought of lambda on each of these, and on the globulin concentration and the ratios of albumin: globulin and albumin: total protein, deduced from these determinations. The only statistically significant regression (P = 0.0004) was that of lambda on the serum triglyceride concentration (T) (mmol/litre): lambda = 1.83 + 0.424T. The dependence of lambda on haemoglobin concentration was not statistically significant, but the slope of the regression was consistent with those of previous investigators. The regressions of lambda, corrected to the mean triglyceride concentration, on the ratios of albumin: globulin and albumin: total protein were not statistically significant but were not significantly different from an earlier reported result.

Anesthesia, Inhalation↗
PubMed1978

Effects of halothane and sodium thiopentone on surface brain pressure and brain electrical impedance in dogs with normal intracranial tension.

The effects of the inhalation of halothane and the i.v. administration of thiopentone on surface brain pressure and brain electrical impedance, at a frequency of 1 kHz, were investigated in 14 chronically implanted dogs. In dogs with normal PaCO2, halothane, at inspired concentrations of 0.8, 1.2, 1.5 and 2.0%, produced increases in brain pressure and impedance. Thiopentone i.v. and hyperventilation preceding the administration of halothane lessened, but did not prevent, the increases in brain pressure and impedance. Thiopentone 35 mg kg-1 decreased both pressure and impedance. The dose-related (P less than 0.01) increase in surface brain pressure was attributed to cerebral vascular expansion; the increase in impedance was not dose related and was interpreted as a loss of conductivity in brain extracellular space (e.c.s.). This loss could be a result of a decrease in both brain e.c.s. volume and its electrolyte concentration resulting from intracellular translocation and electrical inactivation of available ions in brain e.c.s. caused by increased cation binding. These phenomena might be related to the interaction between the anaesthetic molecule and cell proteins. The present study suggests that, in contrast to thiopentone, halothane induced a reversible ionic imbalance in the central nervous system.

Anesthesia, General↗
PubMed1978

Porcine malignant hyperthermia. VI: the effects of bilateral adrenalectomy and pretreatment with bretylium on the halothane-induced response.

The effects of bilateral adrenalectomy, together with the i.v. administration of bretylium tosylate 20 mg kg-1 on halothane-induced malignant hyperthermia (MH), were investigated in six Pietrain pigs. All six animals survived the halothane challenge, and failed to show any signs of increased muscle metabolism. Bilateral adrenalectomy alone prevented halothane-induced MH in three out of four Pietrain pigs, whereas the i.v. administration of bretylium alone protected only one pig out of an additional four animals studied. The results show that complete adrenergic blockade inhibits the susceptibility of Pietrain skeletal muscle to halothane and that the adrenal medulla makes an important contribution to this response.

Adrenalectomy↗
PubMed1979

Failure of clinical concentrations of halothane to block adenosine diphosphate-induced platelet aggregation in vitro.

A dose-related inhibition by halothane of adenosine diphosphate-induced platelet aggregation was measured for human platelets in plasma anticoagulated with sodium citrate 6.8 mmol litre-1 or 13.6 mmol litre-1, or heparin 2 u. ml-1 and for platelets separated from plasma by albumin density gradient centrifugation and requiring no anticoagulant. By maintaining exposure and assay temperature at 37 degrees C, maintaining physiological pH, avoiding age-related deterioration and using an atraumatic equilibration method, no inhibition was found at clinical concentrations of halothane and 50% inhibition required greater than halothane 10%. Sodium citrate, a calcium chelating anticoagulant, was found to enhance halothane inhibition.

Adenosine Diphosphate↗
PubMed1981

Comparison of respiratory characteristics during enflurane and halothane anaesthesia.

The effects of enflurane on certain respiratory characteristics were compared with those of halothane in 70 patients during anaesthesia with spontaneous breathing using a specially designed circuit. The rate of respiration with enflurane (mean 22 b.p.m.) was slower than with halothane (mean 31 b.p.m.; P less than 0.001) and the tidal volume greater (enflurane mean 240 ml, halothane 180 ml; P less than 0.05). There was no statistically significant difference in the minute volume of ventilation or end-tidal carbon dioxide concentration between the two agents. The effects of a narcotic premedication were observed in 16 patients in the study. The main effect was to produce slowing of respiratory rate (enflurane mean 16 b.p.m.; halothane 18 b.p.m.). The value of the respiratory pattern compared with the measurement of heart rate and arterial pressure as a clinical guide during anaesthesia is discussed.

Adolescent↗
PubMed1981

Comparison of halothane and enflurane anaesthesia for otolaryngological surgery in children.

Halothane and enflurane were compared in 131 children undergoing adenoidectomy with or without tonsillectomy. Anaesthesia for adenoidectomy was induced with thiopentone or Althesin and for tonsillectomy with thiopentone. The response to surgery was minimal (0-5%) during both inhalation anaesthetics. During immediate recovery, respiratory depression was more profound after enflurane than after halothane. Both the i.v. and the inhalation anaesthetics had an influence on recovery. The total recovery scores (0-10) based on activity, respiration, heart rate, consciousness and colour improved most rapidly after Althesin + enflurane and most slowly after thiopentone + halothane on the adenoidectomy groups. In the tonsillectomy groups, the recovery scores were better after enflurane than after halothane. After both inhalation anaesthetics, the frequency of shivering ranged from 0 to 17%.

Adenoidectomy↗
PubMed1981

E.C.G changes during halothane and enflurane anaesthesia for E.N.T. surgery in children.

E.c.g. changes were compared in 152 children undergoing adenoidectomy of adenotonsillectomy (T + A) under halothane or enflurane anaesthesia. Junctional rhythm occurred in 4-16% of the children in adenoidectomy groups and in 11-33% in T + A groups. Bundle branch block occurred in 4% of the children anaesthetized with halothane, but not with enflurane and was particularly common in association with thiopentone and T + A operations; one patient had bifocal ventricular tachycardia. QT interval was prolonged compared with control after thiopentone (P less than 0.001) and thiopentone and suxamethonium (P less than 0.02). QT interval was not changed after Althesin with or without suxamethonium. Mean preanaesthetic QT interval (+/- SEM) was significantly prolonged (492 +/- 22 ms; normal 440 ms) in children showing aberrant conduction with chaotic rhythm, but normal (438 +/- 5 ms) when bundle branch block or junctional rhythm was present during halothane anaesthesia. QT interval was prolonged significantly in enflurane but not in halothane anaesthesia.

Adenoidectomy↗
PubMed1983

Myocardial blood flow and oxygen consumption during halothane-nitrous oxide anaesthesia for coronary revascularization.

The effects of halothane on myocardial blood flow and myocardial oxygen balance were studied in seven male patients with stable angina and normal left ventricular function. Patients were receiving maintenance doses of beta-receptor antagonists and underwent coronary artery bypass surgery. Anaesthesia consisted of halothane and 50% nitrous oxide in oxygen. Halothane decreased myocardial blood flow and myocardial oxygen consumption by 29% and 32%, respectively, after induction of anaesthesia, and during sternotomy. Myocardial lactate production was not observed at any time. Cardiac index, stroke volume index, mean arterial pressure and mean diastolic arterial pressure were decreased significantly after induction of anaesthesia and during sternotomy. Heart rate remained unchanged. The global myocardial oxygen supply and demand relationship was maintained. The results suggest that halothane is a safe anaesthetic for coronary revascularization in patients with unimpaired left ventricular function.

Adult↗