This service exclusively searches for literature that cites resources. Please be aware that the total number of searchable documents is limited to those containing RRIDs and does not include all open-access literature.
Etomidate (ET) is a commonly used sedative-hypnotic agent such as propofol to induce anesthesia, and it is rapidly metabolized to etomidate acid (ETA) in liver. Herein, a simple method to determine ET and ETA in urine simultaneously was developed using liquid chromatography-tandem mass spectrometry (LC-MS/MS). A simple sample preparation method reduced the total analysis time. For all analytes, the separation was achieved in 6.5 min using reversed-phase chromatography with gradient elution. The best separation and detection of ETA was achieved using a porous graphitic carbon column. The column temperature was maintained at 30 °C to improve the efficiency and sensitivity. The calibration curves were linear over the concentration ranges of 0.4-120.0 ng/mL (ET) and 1.0-300.0 ng/mL (ETA), obtained with a weighting factor of 1/x2. The coefficients of determination (r2) were greater than 0.9958. The lower limits of quantification were 0.4 ng/mL (ET) and 1.0 ng/mL (ETA), intra-day (n = 6) and inter-day (n = 24) precision values for all compounds were less than 10.2% and 8.4%, respectively, while the intra- and inter-day accuracies were in the -9.9-2.9%, and -7.0-0.6%. The applicability of the method was examined by analyzing the urine samples obtained from ET users.
Etomidate is a preferred drug for the induction of general anesthesia in cardiovascular risk patients. As with propofol and other perioperatively used anesthetics, the application of aqueous etomidate formulations causes an intensive burning pain upon injection. Such algogenic properties of etomidate have been attributed to the solubilizer propylene glycol which represents 35% of the solution administered clinically. The aim of this study was to investigate the underlying molecular mechanisms which lead to injection pain of aqueous etomidate formulations.
Etomidate is a rapid hypnotic intravenous anesthetic agent. The major side effect of etomidate is the reduced plasma concentration of corticosteroids, leading to the abnormal reaction of adrenals. Cortisol and testosterone biosynthesis has similar biosynthetic pathway, and shares several common steroidogenic enzymes, such as P450 side chain cleavage enzyme (CYP11A1) and 3β-hydroxysteroid dehydrogenase 1 (HSD3B1). The effect of etomidate on Leydig cell steroidogenesis during the cell maturation process is not well established.
Etomidate is a hypnotic agent that is used for the induction of anesthesia. It produces its effect by acting as a positive allosteric modulator on the γ-aminobutyric acid type A receptor and thus enhancing the effect of the inhibitory neurotransmitter γ-aminobutyric acid. Etomidate stands out among other anesthetic agents by having a remarkably stable cardiorespiratory profile, producing no cardiovascular or respiratory depression. However, etomidate suppresses the adrenocortical axis by the inhibition of the enzyme 11β-hydroxylase. This makes the drug unsuitable for administration by a prolonged infusion. It also makes the drug unsuitable for administration to critically ill patients. Etomidate has relatively large volumes of distributions and is rapidly metabolized by hepatic esterases into an inactive carboxylic acid through hydrolyzation. Because of the decrease in popularity of etomidate, few modern extensive pharmacokinetic or pharmacodynamic studies exist. Over the last decade, several analogs of etomidate have been developed, with the aim of retaining its stable cardiorespiratory profile, whilst eliminating its suppressive effect on the adrenocortical axis. One of these molecules, ABP-700, was studied in extensive phase I clinical trials. These found that ABP-700 is characterized by small volumes of distribution and rapid clearance. ABP-700 is metabolized similarly to etomidate, by hydrolyzation into an inactive carboxylic acid. Furthermore, ABP-700 showed a rapid onset and offset of clinical effect. One side effect observed with both etomidate and ABP-700 is the occurrence of involuntary muscle movements. The origin of these movements is unclear and warrants further research.
Cognitive impairments following the use of general anesthetics are well documented but the underlying mechanisms are unclear. Here, long-lasting cognitive deficits were observed in aged mice following administration of etomidate at a clinically relevant concentration (20 mg/kg); these deficits were closely related to hippocampal synaptic inhibition and astrocyte dysfunction. Using microdialysis and magnetic-activated cell-sorting techniques, we found that astrocyte secretion of glutamate, d-serine, and ATP, as well as astrocyte function, were depressed in the hippocampus following treatment with etomidate. Interestingly, hippocampal astrocyte inhibition (designer receptors exclusively activated by designer drugs; DREADDs) had no effect on the initial synaptic inhibition, but reversed synaptic and cognitive depression in the long term. Furthermore, continual activation of hippocampal astrocytes following administration of a sedative dose (8 mg/kg) of etomidate induced synaptic inhibition and cognitive dysfunction. Our results indicate that general anesthetic-induced hippocampal astrocyte dysfunction plays a role in maintaining synaptic inhibition, which eventually induces long-lasting cognitive deficits.
Glutamate is the main excitatory neurotransmitter in the vertebrate CNS. Removal of the transmitter from the synaptic cleft by glial and neuronal glutamate transporters (GLTs) has an important function in terminating glutamatergic neurotransmission and neurological disorders. Five distinct excitatory amino-acid transporters have been characterized, among which the glial transporters excitatory amino-acid transporter 1 (EAAT1) (glutamate aspartate transporter) and EAAT2 (GLT1) are most important for the removal of extracellular glutamate. The purpose of this study was to describe the effect of the commonly used anaesthetic etomidate on glutamate uptake in cultures of glial cells.
Objective To investigate the effect of pretreatment with midazolam on myoclonus induced by etomidate injection. Methods A meta-analysis was performed using Review Manager software, version 5.2. Two researchers independently searched PubMed, Cochrane Library, and Embase® databases for randomized controlled trials involving patients who underwent etomidate induced general anaesthesia with or without midazolam pretreatment, published between 1990 and 2016. Outcome measures comprised overall myoclonus incidence rate and incidence rate classified by degree of myoclonus following etomidate injection. Data were assessed using a fixed effects model. Results Five studies, comprising 302 patients, were included for analysis. Overall incidence rate of etomidate injection-induced myoclonus was significantly lower in the pooled midazolam group versus controls (relative risk [RR] 0.34, 95% confidence interval [CI] 0.26, 0.44); Results subgrouped by degree of myoclonus showed significantly lower incidence in midazolam groups versus control groups for mild myoclonus (RR 0.56, 95% CI 0.39, 0.80); moderate myoclonus (RR 0.20, 95% CI 0.10, 0.41); and severe myoclonus (RR 0.12, 95% CI 0.04, 0.39). Conclusion Midazolam can effectively prevent etomidate-induced myoclonus, and alleviate the degree of etomidate-induced myoclonus.
Cushing's syndrome is an endocrine disorder characterized by the overproduction of adrenocortical steroids. Steroidogenesis enzyme inhibitors are the mainstays of pharmacological treatment. Unfortunately, they produce significant side effects. Among the most potent inhibitors is the general anesthetic etomidate whose GABAA receptor-mediated sedative-hypnotic actions restrict use. In this study, we defined the sedative-hypnotic and steroidogenesis inhibiting actions of etomidate and four phenyl-ring substituted etomidate analogs (dimethoxy-etomidate, isopropoxy-etomidate, naphthalene-etomidate, and naphthalene (2)-etomidate) that possess negligible GABAA receptor modulatory activities.
In human, there is substantial neurogenesis in the hippocampus that is implicated in memory formation and learning. These new-born neurons can be affected by neuropathological conditions. Anesthesia and surgical procedures are associated with postoperative cognitive changes particularly, impaired memory and learning. Therefore, the aim of this study was to evaluate the possible neurodegenerative effects of etomidate in rat hippocampus. Thirty male Wistar rats weighing 250 ± 30 g were randomly divided into 3 groups: 1) Etomidate group; four times 20 mg intraperitoneal injection with 1-h intervals, 2) Control group; the equal volume of normal saline, and 3) Normal group; without any intervention. 6 h after the last injection, the brains were removed and processed according to routine histological methods. TUNEL assay and toluidine blue staining were performed to evaluate neuro-histopathological changes in different regions of hippocampus. Our results showed that the number of TUNEL positive cells and dark neurons (DNs) in etomidate group were significantly higher in the CA1, CA2, CA3, and dentate gyrus (DG) of hippocampus compared with the control and normal groups (p < 0.05). While, there was no significant difference between the various regions of hippocampus in control and normal groups. Our findings showed that etomidate can increase apoptotic cells and dark neurons induction in different regions of hippocampus mainly in DG.
Chronic alveolar hypoxia results in sustained arterial constriction, and increase in pulmonary vascular resistance leading to pulmonary artery hypertension (PAHT). The aim of this study was to investigate the effect of propofol and etomidate on pulmonary artery (PA) reactivity in chronically hypoxic (CH) rats, a model of pulmonary arterial hypertension (PAHT), in normoxic animals, and human PA.
Despite its widespread use in North America and many other parts of the world, the safety of etomidate as an induction agent for rapid sequence intubation in septic patients is still debated. In this article, we evaluate the current literature on etomidate, review its clinical history, and discuss the controversy regarding its use, especially in sepsis. We address eight questions: (i) When did concern over the safety of etomidate first arise? (ii) What is the mechanism by which etomidate is thought to affect the adrenal axis? (iii) How has adrenal insufficiency in relation to etomidate use been defined or identified in the literature? (iv) What is the evidence that single dose etomidate is associated with subsequent adrenal-cortisol dysfunction? (v) What is the clinical significance of adrenal insufficiency or dysfunction associated with single dose etomidate, and where are the data that support or refute the contention that single-dose etomidate is associated with increased mortality or important post emergency department (ED) clinical outcomes? (vi) How should etomidate's effects in septic patients best be measured? (vii) What are alternative induction agents and what are the advantages and disadvantages of these agents relative to etomidate? (viii) What future work is needed to further clarify the characteristics of etomidate as it is currently used in patients with sepsis? We conclude that the observational nature of almost all available data suggesting adverse outcomes from etomidate does not support abandoning its use for rapid sequence induction. However, because we see a need to balance theoretical harms and benefits in the presence of data supporting the non-inferiority of alternative agents without similar theoretical risks associated with them, we suggest that the burden of proof to support continued widespread use may rest with the proponents of etomidate. We further suggest that practitioners become familiar with the use of more than one agent while awaiting further definitive data.
This study describes deep sedations performed for painful procedures completed in the emergency department at an academic tertiary care hospital during an 18-month period. One hundred consecutive cases were retrospectively reviewed to describe indications, complications, procedural lengths, medication dosing, and safety of these sedations. Propofol and etomidate were the preferred agents. We found that there were relatively few complications (10%), with only 2 of these (2%) being major complications. All complications were brief and did not adversely affect patient outcomes. This data further demonstrate the safety profile of deep sedation medications in the hands of emergency physicians trained in sedation and advanced airway techniques.
Objective: To evaluate the effect of butorphanol on the prevention of myoclonus induced by etomidate. Materials and methods: We searched the PubMed, Embase, Cochrane Library, and China National Knowledge Infrastructure databases to collect relevant randomized controlled trials (RCTs) evaluating the effect of butorphanol on etomidate-induced myoclonus in January 2019 without any language restrictions. The primary outcome was the incidence of etomidate-induced myoclonus. Secondary outcomes included the incidence of myoclonus at various degrees and the incidence of adverse effects. Risk ratios (RRs) were calculated for binary outcomes. All statistical analysis were performed by using RevMan 5.3 software. Results: We identified 6 RCTs involving a total of 608 patients who reported the incidence of etomidate-induced myoclonus. In pooled analyses, the incidence of etomidate-induced myoclonus in the butorphanol group was significantly lower than that in the control group (RR =0.15, 95% CI [0.10, 0.22], P<0.00001). Subgroup analyses showed that butorphanol significantly decreased the numbers of patients with mild myoclonus (RR =0.41, 95% CI [0.25, 0.68], P=0.0005), moderate myoclonus (RR =0.18, 95% CI [0.09, 0.34], P<0.00001), and severe myoclonus (RR =0.04, 95% CI [0.01, 0.10], P<0.00001). Additionally, butorphanol did not increase the incidence of postoperative nausea/vomiting (RR =3.0, 95% CI [0.32, 28.42], P=0.34) or dizziness (RR =6.79, 95% CI [0.84, 54.84], P=0.07) associated with etomidate. Conclusion: Our findings suggest that butorphanol can effectively prevent the incidence of etomidate-induced myoclonus and alleviate the intensity of etomidate-induced myoclonus, without inducing postoperative nausea/vomiting and dizziness.
Background: Etomidate used for the induction of general anesthesia can result in myoclonus. We tested the hypothesis that pretreatment with dexmedetomidine (Dex) reduces the incidence of etomidate-induced myoclonus during the induction of general anesthesia. Materials and methods: One hundred patients who were scheduled for selective operations under general anesthesia were included in this randomized, double-blind controlled trial. Patients were randomized to receive either Dex 0.5 µg/kg in 20 mL of normal saline or the same volume of normal saline as pretreatment agents 15 mins before the injection of etomidate 0.3 mg/kg. The primary endpoint was the incidence of etomidate-induced myoclonus. Secondary endpoints were the severity of etomidate-induced myoclonus and the incidence of adverse effects from the onset of action of Dex or normal saline to the injection of etomidate, such as dizziness, respiratory depression, bradycardia, hypotension and nausea/vomiting. Results: All of the 100 patients completed the trial. Dex resulted in a significant 38% reduction in the number of patients who experienced etomidate-induced myoclonus: 13 (26%) vs 32 (64%) (P=0.0001). Additionally, the severity of myoclonus was also reduced in the Dex group than that in the placebo group (P=0.02). Incidence of dizziness, respiratory depression, bradycardia, hypotension and nausea/vomiting was similar in both groups. Conclusions: Pretreatment with Dex 0.5 µg/kg 15 mins before the induction of general anesthesia not only resulted in a 38% reduction in the incidence of etomidate-induced myoclonus, but also reduced the severity of myoclonus, without inducing any adverse effects.
Welcome to the FDI Lab - SciCrunch.org Resources search. From here you can search through a compilation of resources used by FDI Lab - SciCrunch.org and see how data is organized within our community.
You are currently on the Community Resources tab looking through categories and sources that FDI Lab - SciCrunch.org has compiled. You can navigate through those categories from here or change to a different tab to execute your search through. Each tab gives a different perspective on data.
If you have an account on FDI Lab - SciCrunch.org then you can log in from here to get additional features in FDI Lab - SciCrunch.org such as Collections, Saved Searches, and managing Resources.
Here is the search term that is being executed, you can type in anything you want to search for. Some tips to help searching:
You can save any searches you perform for quick access to later from here.
We recognized your search term and included synonyms and inferred terms along side your term to help get the data you are looking for.
If you are logged into FDI Lab - SciCrunch.org you can add data records to your collections to create custom spreadsheets across multiple sources of data.
Here are the facets that you can filter your papers by.
From here we'll present any options for the literature, such as exporting your current results.
If you have any further questions please check out our FAQs Page to ask questions and see our tutorials. Click this button to view this tutorial again.
Year:
Count: