TREK-1 and TREK-2 knockout mice are not resistant to halothane or isoflurane. A variety of molecular targets for volatile anesthetics have been suggested including the anesthetic-sensitive K+ leak channel, TREK-1. Knockout of TREK-1 is reported to render mice resistant to volatile anesthetics, making TREK-1 channels compelling targets for anesthetic action. Spinal cord slices from mice, either
Sevoflurane versus halothane for induction of anesthesia in pediatric and adult patients. Induction of anesthesia using an inhalation agent remains a fundamental technique due to its rapid induction and emergence. Sevoflurane is preferred over halothane for its faster induction of anesthesia and lesser complications. Studies on sevoflurane in pediatrics have established it as safe and effective . However, its effectiveness in adults is very limited. Hence, this study was conducted to compare the induction and intubating conditions, hemodynamic profiles, and emergence from anesthesia with sevoflurane and halothane in adults and pediatric patients. This randomized clinical study was carried out for a period of 2 years (November 2006-September 2008) in the Anesthesiology Department of a Krishna
Halothane An official website of the United States government Here's how you know Log inAccess keysNCBI HomepageMyNCBI HomepageMain ContentMain NavigationBookshelfSearch databaseBooksAll DatabasesAssemblyBiocollectionsBioProjectBioSampleBooksClinVarConserved DomainsdbGaPdbVarGeneGenomeGEO DataSetsGEO ProfilesGTRHomoloGeneIdentical Protein GroupsMedGenMeSHNLM and EffectsSummary of Use during LactationHalothane is no longer available in the United States. There is no published experience with the therapeutic use of halothane as an anesthetic during breastfeeding, but trace amounts were found in the milk of a practicing anesthesiologist who had administered halothane in the operating room. Various recommendations have been made regarding breastfeeding after halothane
Competitive Interactions between Halothane and Isoflurane at the Carotid Body and TASK Channels. The degree to which different volatile anesthetics depress carotid body hypoxic response relates to their ability to activate TASK potassium channels. Most commonly, volatile anesthetic pairs act additively at their molecular targets. We examined whether this applied to carotid body TASK channels. We studied halothane and isoflurane effects on hypoxia-evoked rise in intracellular calcium (Ca2+i, using the indicator Indo-1) in isolated neonatal rat glomus cells, and TASK single-channel activity (patch clamping) in native glomus cells and HEK293 cell line cells transiently expressing TASK-1. Halothane (5%) depressed glomus cell Ca2+i hypoxic response (mean ± SD, 94 ± 4% depression; P < 0.001 vs
Abnormal calcium signalling and the caffeine-halothane contracture test. The variable clinical presentation of malignant hyperthermia (MH), a disorder of calcium signalling, hinders its diagnosis and management. Diagnosis relies on the caffeine-halothane contracture test, measuring contraction forces upon exposure of muscle to caffeine or halothane (F and F, respectively). Patients with above -threshold F or F are diagnosed as MH susceptible. Many patients test positive to halothane only (termed 'HH'). Our objective was to determine the characteristics of these HH patients, including their clinical symptoms and features of cytosolic Ca signalling related to excitation-contraction coupling in myotubes. After institutional ethics committee approval, recruited patients undergoing contracture
Voltage modulates halothane-triggered Ca2+ release in malignant hyperthermia-susceptible muscle Malignant hyperthermia (MH) is a fatal hypermetabolic state that may occur during general anesthesia in susceptible individuals. It is often caused by mutations in the ryanodine receptor RyR1 that favor drug-induced release of Ca from the sarcoplasmic reticulum. Here, knowing that membrane depolarization triggers Ca release in normal muscle function, we study the cross-influence of membrane potential and anesthetic drugs on Ca release. We used short single muscle fibers of knock-in mice heterozygous for the RyR1 mutation Y524S combined with microfluorimetry to measure intracellular Ca signals. Halothane, a volatile anesthetic used in contracture testing for MH susceptibility, was equilibrated
Effects of halothane on the electroencephalogram of the chicken Little is known about the effects of inhalant anaesthetics on the avian electroencephalogram (EEG). The effects of halothane on the avian EEG are of interest, as this agent has been widely used to study nociception and analgesia in mammals. The objective of this study was to characterize the effects of halothane anaesthesia on the EEG of the chicken. Twelve female Hyline Brown chickens aged 8-10 weeks were anaesthetized with halothane in oxygen. For each bird, anaesthesia was progressively increased from 1-1.5 to 2 times the Minimum Anesthetic Concentration (MAC), then progressively decreased again. At each concentration, a sample of EEG was recorded after a 10-min stabilization period. The mean Total Power (P ), Median
Isoflurane but Not Halothane Prevents and Reverses Helpless Behavior: A Role for EEG Burst Suppression? The volatile anesthetic isoflurane may exert a rapid and long-lasting antidepressant effect in patients with medication-resistant depression. The mechanism underlying the putative therapeutic actions of the anesthetic have been attributed to its ability to elicit cortical burst suppression , a distinct EEG pattern with features resembling the characteristic changes that occur following electroconvulsive therapy. It is currently unknown whether the antidepressant actions of isoflurane are shared by anesthetics that do not elicit cortical burst suppression. In vivo electrophysiological techniques were used to determine the effects of isoflurane and halothane, 2 structurally unrelated volatile
Effect of bispectral index versus end-tidal anesthetic gas concentration-guided protocol on time to tracheal extubation for halothane-based general anesthesia. Early extubation is a desirable goal after general anesthesia. Very few studies have compared the effect of bispectral index (BIS) monitoring versus standard end-tidal anesthetic gas (ETAG) concentration monitoring on tracheal extubation time for halothane-based anesthesia. The aim of this study was to compare the effect of BIS versus ETAG-guided anesthesia on time to tracheal extubation for halothane-based anesthesia in general surgical setting. This was a randomized, controlled double-blind study. Sixty patients with the American Society of Anesthesiologists physical status Class 1 or 2, receiving halothane-based general anesthesia
Effect of sevoflurane and halothane anesthesia on cognitive function and immune function in young rats In the current study, we scrutinized the effect of sevoflurane and halothane on cognitive and immune function in young rats. The rats were divided into following groups: sevoflurane, halothane and sevoflurane + halothane groups, respectively. The rats were regularly treated with the pre -determined treatment. We also scrutinized the serum proinflammatory cytokines including IL-10, IL-4 and IL-2; brain level IL-1β; hippocampal neuronal apoptosis concentration were estimated. The water maze test was performed in rats for the estimation of cognitive ability. During the water maze test, on the 1st day the sevoflurane group showed the latency; sevoflurane and sevoflurane + halothane group
Comparative Study of Recovery after Sevoflurane versus Halothane Anaesthesia in Adult Patients. Induction and maintenance characteristics of sevoflurane and halothane have been studied, but little work has been done to compare the postoperative recovery of these two agents. Sixty adult, ASA I and II patients were allocated randomly into Group A and Group B of 30 each. Group A received sevoflurane and Group B received halothane for maintenance. At the end of surgery early recovery, intermediate recovery and discharge criteria were assessed. Early recovery assessed with the mean time to extubation was 6.7 ± 2.29 min in Group A and 9.07 ± 1.64 min in Group B; eye opening was 7.28 ± 2.3 min in Group A and 10.6 ± 1.77 min in Group B; response to verbal command was 8.52 ± 2.83 min in Group
Drug-induced allergic hepatitis developed in mice when myeloid-derived suppressor cells were depleted prior to halothane treatment. Clinical evidence suggests that many cases of serious idiosyncratic drug-induced liver injury are mediated by the adaptive immune system in response to hepatic drug-protein adducts, also referred to as "drug-induced allergic hepatitis"; but detailed mechanistic proof has remained elusive due to the lack of animal models. We have hypothesized that drug-induced allergic hepatitis is as rare in animals as it is in humans due at least in part to the tolerogenic nature of the liver. We provide evidence that immune tolerance can be overcome in a murine model of halothane-induced liver injury initiated by trifluoroacetylated protein adducts of halothane formed
Antioxidants Protect Calsequestrin-1 Knockout Mice from Halothane- and Heat-induced Sudden Death. Mice lacking calsequestrin-1 (CASQ1-null), a Ca-binding protein that modulates the activity of Ca release in the skeletal muscle, exhibit lethal hypermetabolic episodes that resemble malignant hyperthermia in humans when exposed to halothane or heat stress. Because oxidative species may play a critical role in malignant hyperthermia crises, we treated CASQ1-null mice with two antioxidants, N-acetylcysteine (NAC, Sigma-Aldrich, Italy; provided ad libitum in drinking water) and (±)-6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid (Trolox, Sigma-Aldrich; administered by intraperitoneal injection), before exposure to halothane (2%, 1 h) or heat (41°C, 1 h). NAC and Trolox significantly
Halothane Modulates the Type I Interferon Response to Influenza and Minimizes the Risk of Secondary Bacterial Pneumonia through Maintenance of Neutrophil Recruitment in an Animal Model. To minimize the risk of pneumonia, many anesthesiologists delay anesthesia-requiring procedures when patients exhibit signs of viral upper respiratory tract infection. Postinfluenza secondary bacterial pneumonias (SBPs) are a major cause of morbidity and mortality. An increased host susceptibility to SBP postinfluenza has been attributed to physical damage to the pulmonary epithelium, but flu-induced effects on the immune system are being shown to also play an important role. The authors demonstrate that halothane mitigates the risk of SBP postflu through modulation of the effects of type I interferon (IFN
Emulsified halothane produces long-term epidural anesthetic effect: a study in rabbits. Previous studies have demonstrated that volatile anesthetics could produce local anesthesia. Emulsified isoflurane at 8% has been reported to produce epidural anesthetic effect in rabbits. This study was designed to investigate the long-term epidural anesthetic effect of emulsified halothane in rabbits . In this study, 40 healthy adult rabbits (weighting 2.0-2.5 kg) with an epidural catheter were randomly divided into 4 groups (n=10/group), receiving epidural administration of 1% lidocaine (lido group), 8% emulsified isoflurane 1ml (8% E-iso group), 8% emulsified halothane (8% E-Halo group) and 12% emulsified halothane (12% E-Halo group). After administration, sensory and motor functions as well
Thymic Stromal Lymphopoietin and Interleukin-4 Mediate the Pathogenesis of Halothane-Induced Liver Injury in Mice. Liver eosinophilia has been associated with incidences of drug-induced liver injury (DILI) for more than 50 years, although its role in this disease has remained largely unknown. In this regard, it was recently shown that eosinophils played a pathogenic role in a mouse model of halothane-induced liver injury (HILI). However, the signaling events that drove hepatic expression of eosinophil-associated chemokines, eotaxins, eosinophil infiltration, and subsequent HILI were unclear. We now provide evidence implicating hepatic epithelial-derived cytokine thymic stromal lymphopoietin (TSLP) and type 2 immunity, in particular, interleukin-4 (IL-4) production, in mediating hepatic