A potent benzodiazepine receptor antagonist. Since it reverses the sedative and other actions of benzodiazepines, it has been suggested as an antidote to benzodiazepine overdoses.
Substances that do not act as agonists or antagonists but do affect the GAMMA-AMINOBUTYRIC ACID receptor-ionophore complex. GABA-A receptors (RECEPTORS, GABA-A) appear to have at least three allosteric sites at which modulators act: a site at which BENZODIAZEPINES act by increasing the opening frequency of GAMMA-AMINOBUTYRIC ACID-activated chloride channels; a site at which BARBITURATES act to prolong the duration of channel opening; and a site at which some steroids may act. GENERAL ANESTHETICS probably act at least partly by potentiating GABAergic responses, but they are not included here.
A short-acting hypnotic-sedative drug with anxiolytic and amnestic properties. It is used in dentistry, cardiac surgery, endoscopic procedures, as preanesthetic medication, and as an adjunct to local anesthesia. The short duration and cardiorespiratory stability makes it useful in poor-risk, elderly, and cardiac patients. It is water-soluble at pH less than 4 and lipid-soluble at physiological pH.
A benzodiazepine with anticonvulsant, anxiolytic, sedative, muscle relaxant, and amnesic properties and a long duration of action. Its actions are mediated by enhancement of GAMMA-AMINOBUTYRIC ACID activity.
Cell surface proteins which bind GAMMA-AMINOBUTYRIC ACID and contain an integral membrane chloride channel. Each receptor is assembled as a pentamer from a pool of at least 19 different possible subunits. The receptors belong to a superfamily that share a common CYSTEINE loop.
A group of two-ring heterocyclic compounds consisting of a benzene ring fused to a diazepine ring.
Agents counteracting or neutralizing the action of POISONS.
Drugs that bind to but do not activate GABA-A RECEPTORS thereby blocking the actions of endogenous or exogenous GABA-A RECEPTOR AGONISTS.
Agents that alleviate ANXIETY, tension, and ANXIETY DISORDERS, promote sedation, and have a calming effect without affecting clarity of consciousness or neurologic conditions. ADRENERGIC BETA-ANTAGONISTS are commonly used in the symptomatic treatment of anxiety but are not included here.
A drug-induced depression of consciousness during which patients respond purposefully to verbal commands, either alone or accompanied by light tactile stimulation. No interventions are required to maintain a patent airway. (From: American Society of Anesthesiologists Practice Guidelines)
A short-acting benzodiazepine used in the treatment of insomnia. Some countries temporarily withdrew triazolam from the market because of concerns about adverse reactions, mostly psychological, associated with higher dose ranges. Its use at lower doses with appropriate care and labeling has been reaffirmed by the FDA and most other countries.
A group of pyrido-indole compounds. Included are any points of fusion of pyridine with the five-membered ring of indole and any derivatives of these compounds. These are similar to CARBAZOLES which are benzo-indoles.
A range of methods used to reduce pain and anxiety during dental procedures.
Endogenous compounds and drugs that bind to and activate GABA-A RECEPTORS.
An anxiolytic benzodiazepine derivative with anticonvulsant, sedative, and amnesic properties. It has also been used in the symptomatic treatment of alcohol withdrawal.
Abnormally slow pace of regaining CONSCIOUSNESS after general anesthesia (ANESTHESIA, GENERAL) usually given during surgical procedures. This condition is characterized by persistent somnolence.
The period of emergence from general anesthesia, where different elements of consciousness return at different rates.
Drugs used to induce drowsiness or sleep or to reduce psychological excitement or anxiety.
A pyrazolodiazepinone with pharmacological actions similar to ANTI-ANXIETY AGENTS. It is commonly used in combination with TILETAMINE to obtain immobilization and anesthesia in animals.
A benzodiazepine with pharmacologic actions similar to those of DIAZEPAM that can cause ANTEROGRADE AMNESIA. Some reports indicate that it is used as a date rape drug and suggest that it may precipitate violent behavior. The United States Government has banned the importation of this drug.
Proposed anesthetic with possible anticonvulsant and sedative properties.
A benzodiazepine used as an anti-anxiety agent with few side effects. It also has hypnotic, anticonvulsant, and considerable sedative properties and has been proposed as a preanesthetic agent.
A pregnane found in the urine of pregnant women and sows. It has anesthetic, hypnotic, and sedative properties.
The sodium salt of 4-hydroxybutyric acid. It is used for both induction and maintenance of ANESTHESIA.
Unstable isotopes of carbon that decay or disintegrate emitting radiation. C atoms with atomic weights 10, 11, and 14-16 are radioactive carbon isotopes.
Benzodiazepinones are a class of psychoactive drugs that bind to the GABA-A receptor and enhance its inhibitory effects, producing anxiolytic, sedative, hypnotic, anticonvulsant, and muscle relaxant properties.
A profound state of unconsciousness associated with depressed cerebral activity from which the individual cannot be aroused. Coma generally occurs when there is dysfunction or injury involving both cerebral hemispheres or the brain stem RETICULAR FORMATION.
A central respiratory stimulant with a brief duration of action. (From Martindale, The Extra Pharmocopoeia, 30th ed, p1225)
The relationship between the dose of an administered drug and the response of the organism to the drug.
Endogenous compounds and drugs that bind to and activate GAMMA-AMINOBUTYRIC ACID receptors (RECEPTORS, GABA).
Tomography using radioactive emissions from injected RADIONUCLIDES and computer ALGORITHMS to reconstruct an image.
Physiological and psychological symptoms associated with withdrawal from the use of a drug after prolonged administration or habituation. The concept includes withdrawal from smoking or drinking, as well as withdrawal from an administered drug.
A pharmaceutical agent that displays activity as a central nervous system and respiratory stimulant. It is considered a non-competitive GAMMA-AMINOBUTYRIC ACID antagonist. Pentylenetetrazole has been used experimentally to study seizure phenomenon and to identify pharmaceuticals that may control seizure susceptibility.

Regional differences in the inhibition of mouse in vivo [3H]Ro 15-1788 binding reflect selectivity for alpha 1 versus alpha 2 and alpha 3 subunit-containing GABAA receptors. (1/376)

The benzodiazepines flunitrazepam, diazepam, and Ro 15-1788 and the beta-carboline DMCM bind with equivalent affinity to the benzodiazepine binding site of GABAA receptors containing different alpha subunits (i.e., alpha 1, alpha 2, alpha 3, or alpha 5); whereas, the triazolopyridazine CL 218,872 and imidazopyridine zolpidem have higher affinity for alpha 1 subunit-containing GABAA receptors. In the present study, the in vivo binding of [3H]Ro 15-1788 in mouse cerebellum and spinal cord was used to establish the occupancy of the benzodiazepine binding site of GABAA receptors containing primarily alpha 1 and alpha 2/alpha 3 subunits, respectively. Thus, the nonselective compounds flunitrazepam, diazepam, and DMCM all produced a similar inhibition of binding in cerebellum and spinal cord (respective ID50 values of 0.2 to 0.3 mg/kg, 2 mg/kg, and 10 mg/kg i.p.); whereas, the alpha 1 selective compounds CL 218,872 and zolpidem were more potent at inhibiting [3H]Ro 15-1788 binding in the cerebellum (ID50 values 4.5 mg/kg and 10 mg/kg i.p.) compared to the spinal cord (ID50 values 12 mg/kg and > 30 mg/kg i.p.). Thus, the reduction of in vivo f[3H]Ro 15-1788 binding in tissues containing alpha 1 and alpha 2/alpha 3 receptor populations reflects the in vitro affinities of subtype selective compounds and should help to interpret the behavioral profile of such compounds.  (+info)

Stoichiometry of a ligand-gated ion channel determined by fluorescence energy transfer. (2/376)

We have developed a method to determine the stoichiometry of subunits within an oligomeric cell surface receptor using fluorescently tagged antibodies to the individual subunits and measuring energy transfer between them. Anti-c-Myc monoclonal antibody (mAb 9-E10) derivatized with a fluorophore (europium cryptate, EuK) was used to individually label c-Myc-tagged alpha1-, beta2-, or gamma2-subunits of the hetero-oligomeric gamma-aminobutyric acid (GABAA) receptor in intact cells. The maximal fluorescent signal derived from the alpha1(c-Myc)beta2gamma2 and the alpha1beta2(c-Myc)gamma2 receptors was twice that obtained with alpha1beta2gamma2(c-Myc), suggesting that there are 2x alpha-, 2x beta-, and 1x gamma-subunits in a receptor monomer. This observation was extended using fluorescence energy transfer. Receptors were half-maximally saturated with EuK-anti-c-Myc mAb, and the remaining alpha1(c-Myc) subunits were labeled with excess anti-c-Myc mAb derivatized with the fluorescence energy acceptor, XL665. On exposure to laser light, energy transfer from EuK to XL665 occurred with alpha1(c-Myc)beta2gamma2 and alpha1beta2(c-Myc)gamma2, but no significant energy transfer was observed with alpha1beta2gamma2(c-Myc) receptors, indicating the absence of a second gamma-subunit in a receptor monomer. We confirm that the GABAA receptor subtype, alpha1beta2gamma2, is composed of two copies each of the alpha- and beta-subunits and one copy of the gamma-subunit (i.e. (alpha1)2(beta2)2(gamma2)1) and conclude that this method would have general applicability to other multisubunit cell surface proteins.  (+info)

Midazolam effects on prepulse inhibition of the acoustic blink reflex. (3/376)

AIMS: The eye-blink response following sudden acoustic noise bursts is part of the startle reflex. The magnitude of the startle response can be attenuated by presentation of a weak stimulus before the 'startle-eliciting' stimulus (prepulse inhibition, PPI). PPI is a stable finding in awake humans but may be altered by anaesthetic drugs. We investigated whether the application of benzodiazepines altered the magnitude of PPI in healthy male volunteers. METHODS: In an open-label noncontrolled investigation, the effect of the benzodiazepine agonist midazolam on PPI was assessed in the absence and presence of the antagonist flumazenil. After an initial control period of 60 min three consecutive periods, each of 60 min, with progressively increasing concentrations of midazolam were studied (0. 02, 0.06, 0.14 mg kg-1 h-1 ). A final 60 min period during the administration of flumazenil (0.004 mg kg-1 h-1 ) and while the agonist was still present was also studied. Drug was administered intravenuously as a combination of bolus, 50% of total dose and continuous infusion over the 60 min period. Electromyographic (EMG) response of the right orbicularis oculi muscle was used to assess the startle response to noise bursts of 50 ms duration (95 dB(A)). Noise bursts were randomly preceded by nonstartling prepulses (800 Hz sinus, 50 ms duration, 65 dB(A), prepulse to noise interval 120 ms). The magnitude of PPI was calculated by dividing the EMG response to nonprepulsed stimuli by the response to prepulsed stimuli for each individual and period. Eleven subjects participated in the study, two of them were excluded from the statistical analysis because startle responses could not be reliably elicited (final sample size n=9). RESULTS: The magnitude of PPI was inversely related to the concentration of midazolam. This relationship was described by a sigmoidal Emax model, giving an Emax of 0.65+/-0.13, an ED50 of 33.9+/-10.9 ng ml-1 and gamma of 3.5+/-1.0. During infusion of flumazenil and in the presence of midazolam, the magnitude of PPI increased by 0.11 (95% CI, 0-0.22, P+info)

No evidence of altered in vivo benzodiazepine receptor binding in schizophrenia. (4/376)

Deficits in gamma-amino-butyric acid (GABA) neurotransmitter systems have been implicated in the pathophysiology of schizophrenia for more than two decades. Previous postmortem and in vivo studies of benzodiazepine (BDZ) receptor density have reported alterations in several brain regions of schizophrenic patients. The goal of this study was to better characterize possible alterations of the in vivo regional distribution volume (VT) of BDZ receptors in schizoprenia, using the selective BDZ antagonist [123I]iomazenil and single photon emission computerized tomography (SPECT). Regional BDZ VT was measured under sustained radiotracer equilibrium conditions. The reproducibility and reliability of this measurement was established in four healthy volunteers. No differences in regional BDZ VT were observed between 16 male schizophrenic patients and 16 matched controls. No relationships were observed between BDZ VT and severity of psychotic symptoms in any of the regions examined. In conclusion, this study failed to identify alterations of BDZ receptors density in schizoprenia. If this illness is associated with deficits in GABA transmission, these deficits do not substantially involve BDZ receptor expression or regulation.  (+info)

Acute pentylenetetrazol injection reduces rat GABAA receptor mRNA levels and GABA stimulation of benzodiazepine binding with No effect on benzodiazepine binding site density. (5/376)

The effects of a single convulsive dose of pentylenetetrazol (PTZ, 45 mg/kg i.p.) on rat brain gamma-aminobutyric acid type A (GABAA) receptors were studied. Selected GABAA receptor subunit mRNAs were measured by Northern blot analysis (with beta-actin mRNA as a standard). Four hours after PTZ, the GABAA receptor gamma2-mRNA was decreased in hippocampus, cerebral cortex, and cerebellum; alpha1-mRNA was decreased in cerebellum; and beta2 subunit mRNA was decreased in cortex and cerebellum. The alpha5 subunit mRNA level was not altered. Those mRNAs that had been reduced were increased in some brain regions at the 24-h time point, and these changes reverted to control levels by 48 h. PTZ effect on GABAA receptors was also studied by autoradiographic binding assay with the benzodiazepine agonist [3H]flunitrazepam (FNP), the GABAA agonist [3H]muscimol, and the benzodiazepine antagonist [3H]flumazenil. There was an overall decrease in [3H]FNP binding 12 but not 24 h after PTZ treatment. In contrast, [3H]muscimol binding was minimally affected, and [3H]flumazenil binding was unchanged after PTZ treatment. Additional binding studies were performed with well-washed cerebral cortical homogenates to minimize the amount of endogenous GABA. There was no PTZ effect on specific [3H]FNP binding. However, there was a significant reduction in the stimulation of [3H]FNP binding by GABA. The results showed that an acute injection of PTZ caused transient changes in GABAA receptor mRNA levels without altering receptor number but affected the coupling mechanism between the GABA and benzodiazepine sites of the GABAA receptor.  (+info)

Native gamma-aminobutyric acid type A receptors from rat hippocampus, containing both alpha 1 and alpha 5 subunits, exhibit a single benzodiazepine binding site with alpha 5 pharmacological properties. (6/376)

Evidences indicate the existence of two homologous and/or heterologous alpha subunits coassembled in a single gamma-aminobutyric acid type A (GABA(A)) receptor. However, it is unknown whether both or only one of the coassembled alpha subunits display benzodiazepine binding sites. Thus, we have investigated the association between alpha1 and alpha5 subunits and the pharmacological properties of these GABA(A) receptors from rat hippocampus. The association between alpha1 and alpha5 subunits was demonstrated by immunoblot of the anti-alpha1 or -alpha5 immunoaffinity-purified receptors and by double immunopurification by anti-alpha1 and -alpha5 columns in series. The benzodiazepine binding properties of the immunoprecipitated receptors indicated the existence of pharmacologically active and inactive alpha subunits. The anti-alpha5 immunoprecipitated receptors displayed exclusively low-affinity binding sites for both Cl218,872 (K(i) = 0.81 +/- 0.15 microM) and zolpidem (K(i) = 5.0 +/- 3.0 microM), in spite of the association between alpha1 and alpha5 subunits. The anti-alpha1 immunoprecipitated receptors displayed both high- and low-affinity binding sites for both ligands (K(i)s = 47.5 +/- 5.2 nM and 0.7 +/- 0.06 microM for Cl218,872 and 25.0 +/- 7.0 nM, 415 +/- 200 nM and 9. 3 +/- 3.0 microM for zolpidem). Therefore, the alpha5 subunit, when coassembled with alpha1 subunit, should be pharmacologically predominant. This hypothesis was probed by immunoprecipitation of the photoaffinity-labeled receptors and by anti-alpha1 and -alpha5 double immunopurified receptors. The alpha1-alpha5 double immunopurified receptors displayed a single low-affinity binding site (K(i) = 908 +/- 105 nM) for Cl218,872, undetectable [(3)H]zolpidem binding activity, and similar [(3)H]flumazenil and [(3)H]L-655,708 binding activity (0.10 +/- 0.01 and 0.09 +/- 0.02 pmol/20 microliters of anti-alpha5 immunobeads, respectively). Thus, the native GABA(A) receptors containing alpha1 and alpha5 subunits have only one alpha subunit pharmacologically active displaying alpha5 binding properties.  (+info)

Apparent pA2 values of benzodiazepine antagonists and partial agonists in monkeys. (7/376)

Drugs that bind to benzodiazepine recognition sites of gamma-aminobutyric acid type A receptor complexes may function as agonists in some behavioral assays and as antagonists in other behavioral assays. The present studies compared the effects of the benzodiazepines midazolam, flumazenil, bretazenil, Ro 41-7812, and Ro 42-8773 and the beta-carboline, beta-carboline-3-carboxylate-t-butyl ester (beta-CCt) under two different types of schedule-controlled responding in squirrel monkeys. One group of monkeys responded under a fixed-ratio schedule of stimulus-shock termination, and a second group of monkeys responded under a multiple fixed-ratio schedule of food presentation involving suppressed and nonsuppressed behavior. Under the schedule of stimulus-shock termination, midazolam produced dose-related decreases in response rate, and these effects were surmountably antagonized by flumazenil, bretazenil, Ro 41-7812, Ro 42-8773, and beta-CCt. Schild plot analysis of these data revealed the following mean pA(2) values: flumazenil, 7.18; bretazenil, 7.62; Ro 41-7812, 7. 06; Ro 42-8773, 6.95. Apparent pA(2) values were not calculated for beta-CCt because the CL of the slope of the Schild plot included positive values. Under the multiple schedule, midazolam, bretazenil, and Ro 42-8773 dose-dependently increased rates of suppressed responding, whereas flumazenil, Ro 41-7812, and beta-CCt had no significant rate-altering effects. Flumazenil antagonized the antisuppressant effects of midazolam and bretazenil; however, individual variability in these effects prohibited the determination of apparent pA(2) values. These results indicate that in vivo pA(2) values may be determined for benzodiazepine-site ligands. These results further demonstrate that some benzodiazepine-site ligands, e. g., bretazenil and Ro 42-8773, may function as both agonists and as competitive antagonists in vivo.  (+info)

Altered in vitro and in vivo flumazenil binding in human epileptogenic neocortex. (8/376)

In vitro and in vivo parameters of flumazenil (FMZ) binding were measured in spiking and nonspiking neocortex identified by intraoperative electrocorticography in epileptic patients who underwent cortical resection for seizure control. In vitro measures of receptor affinity (K(D)), number (Bmax) and laminar distribution for [3H]-FMZ binding in the epileptic focus (n = 38) were compared to nonspiking cortex from a subgroup of the patients (n = 12) and to tissue obtained from trauma patients (n = 5). The in vitro binding parameters were compared to in vivo [11C]-FMZ binding measured with positron emission tomography (PET) (n = 19). The Bmax was higher in the 38 spiking tissues as compared to the 12 nonspiking tissues (P = .012). Paired comparison of spiking versus nonspiking binding in the 12 patients from whom nonspiking tissue was available showed increases in both K(D) (P = .037) and Bmax (P = .0047) in spiking cortex. A positive correlation was found between K(D) and Bmax values for 38 patients (r = 0.55, P < .0001), the magnitude of the K(D) increase being twice that of the Bmax increase. In addition, there was a significant correlation between the asymmetry indices of the in vivo FMZ binding on PET and in vitro K(D) of spiking cortex (n = 19, r = 0.52, P = .02). The laminar distribution of [3H]-FMZ showed increased FMZ binding in cortical layers V-VI in spiking cortex compared to nonspiking and control cortex. The increased receptor number in spiking cortical layers V-VI may be a compensatory mechanism to decreased GABAergic input. The increased Bmax in spiking cortex was accompanied by a larger decrease in the affinity of FMZ for the receptor suggesting that decreased FMZ binding in the epileptic focus measured with PET is due to a decrease in the affinity of the tracer for the receptor.  (+info)

Flumazenil is a medication that acts as a competitive antagonist at benzodiazepine receptors. It is primarily used in clinical settings to reverse the effects of benzodiazepines, which are commonly prescribed for their sedative, muscle relaxant, and anxiety-reducing properties. Flumazenil can reverse symptoms such as excessive sedation, respiratory depression, and impaired consciousness caused by benzodiazepine overdose or adverse reactions. It is important to note that flumazenil should be administered with caution, as it can precipitate seizures in individuals who are physically dependent on benzodiazepines.

GABA (gamma-aminobutyric acid) modulators are substances that affect the function of GABA, which is the primary inhibitory neurotransmitter in the central nervous system. GABA plays a crucial role in regulating neuronal excitability and reducing the activity of overactive nerve cells.

GABA modulators can either enhance or decrease the activity of GABA receptors, depending on their specific mechanism of action. These substances can be classified into two main categories:

1. Positive allosteric modulators (PAMs): These compounds bind to a site on the GABA receptor that is distinct from the neurotransmitter binding site and enhance the activity of GABA at the receptor, leading to increased inhibitory signaling in the brain. Examples of positive allosteric modulators include benzodiazepines, barbiturates, and certain non-benzodiazepine drugs used for anxiolysis, sedation, and muscle relaxation.
2. Negative allosteric modulators (NAMs): These compounds bind to a site on the GABA receptor that reduces the activity of GABA at the receptor, leading to decreased inhibitory signaling in the brain. Examples of negative allosteric modulators include certain antiepileptic drugs and alcohol, which can reduce the effectiveness of GABA-mediated inhibition and contribute to their proconvulsant effects.

It is important to note that while GABA modulators can have therapeutic benefits in treating various neurological and psychiatric conditions, they can also carry risks for abuse, dependence, and adverse side effects, particularly when used at high doses or over extended periods.

Midazolam is a medication from the class of drugs known as benzodiazepines. It works by enhancing the effect of a neurotransmitter called gamma-aminobutyric acid (GABA), which has a calming effect on the brain and nervous system. Midazolam is often used for its sedative, hypnotic, anxiolytic, anticonvulsant, and muscle relaxant properties.

Medically, midazolam is used for various purposes, including:

1. Preoperative medication (sedation before surgery)
2. Procedural sedation (for minor surgical or diagnostic procedures)
3. Treatment of seizures (status epilepticus)
4. Sedation in critically ill patients
5. As an adjunct to anesthesia during surgeries
6. Treatment of alcohol withdrawal symptoms
7. To induce amnesia for certain medical or dental procedures

Midazolam is available in various forms, such as tablets, intravenous (IV) solutions, and intranasal sprays. It has a rapid onset of action and a short duration, making it suitable for brief, intermittent procedures. However, midazolam can cause side effects like drowsiness, confusion, respiratory depression, and memory impairment. Therefore, its use should be carefully monitored by healthcare professionals.

Diazepam is a medication from the benzodiazepine class, which typically has calming, sedative, muscle relaxant, and anticonvulsant properties. Its medical uses include the treatment of anxiety disorders, alcohol withdrawal syndrome, end-of-life sedation, seizures, muscle spasms, and as a premedication for medical procedures. Diazepam is available in various forms, such as tablets, oral solution, rectal gel, and injectable solutions. It works by enhancing the effects of a neurotransmitter called gamma-aminobutyric acid (GABA) in the brain, which results in the modulation of nerve impulses in the brain, producing a sedative effect.

It is important to note that diazepam can be habit-forming and has several potential side effects, including drowsiness, dizziness, weakness, and impaired coordination. It should only be used under the supervision of a healthcare professional and according to the prescribed dosage to minimize the risk of adverse effects and dependence.

GABA-A receptors are ligand-gated ion channels in the membrane of neuronal cells. They are the primary mediators of fast inhibitory synaptic transmission in the central nervous system. When the neurotransmitter gamma-aminobutyric acid (GABA) binds to these receptors, it opens an ion channel that allows chloride ions to flow into the neuron, resulting in hyperpolarization of the membrane and decreased excitability of the neuron. This inhibitory effect helps to regulate neural activity and maintain a balance between excitation and inhibition in the nervous system. GABA-A receptors are composed of multiple subunits, and the specific combination of subunits can determine the receptor's properties, such as its sensitivity to different drugs or neurotransmitters.

Benzodiazepines are a class of psychoactive drugs that have been widely used for their sedative, hypnotic, anxiolytic, anticonvulsant, and muscle relaxant properties. They act by enhancing the inhibitory effects of gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the central nervous system.

Benzodiazepines are commonly prescribed for the treatment of anxiety disorders, insomnia, seizures, and muscle spasms. They can also be used as premedication before medical procedures to produce sedation, amnesia, and anxiolysis. Some examples of benzodiazepines include diazepam (Valium), alprazolam (Xanax), clonazepam (Klonopin), lorazepam (Ativan), and temazepam (Restoril).

While benzodiazepines are effective in treating various medical conditions, they can also cause physical dependence and withdrawal symptoms. Long-term use of benzodiazepines can lead to tolerance, meaning that higher doses are needed to achieve the same effect. Abrupt discontinuation of benzodiazepines can result in severe withdrawal symptoms, including seizures, hallucinations, and anxiety. Therefore, it is important to taper off benzodiazepines gradually under medical supervision.

Benzodiazepines are classified as Schedule IV controlled substances in the United States due to their potential for abuse and dependence. It is essential to use them only as directed by a healthcare provider and to be aware of their potential risks and benefits.

An antidote is a substance that can counteract the effects of a poison or toxin. It works by neutralizing, reducing, or eliminating the harmful effects of the toxic substance. Antidotes can be administered in various forms such as medications, vaccines, or treatments. They are often used in emergency situations to save lives and prevent serious complications from poisoning.

The effectiveness of an antidote depends on several factors, including the type and amount of toxin involved, the timing of administration, and the individual's response to treatment. In some cases, multiple antidotes may be required to treat a single poisoning incident. It is important to note that not all poisons have specific antidotes, and in such cases, supportive care and symptomatic treatment may be necessary.

Examples of common antidotes include:

* Naloxone for opioid overdose
* Activated charcoal for certain types of poisoning
* Digoxin-specific antibodies for digoxin toxicity
* Fomepizole for methanol or ethylene glycol poisoning
* Dimercaprol for heavy metal poisoning.

GABA-A receptor antagonists are pharmacological agents that block the action of gamma-aminobutyric acid (GABA) at GABA-A receptors. GABA is the primary inhibitory neurotransmitter in the central nervous system, and it exerts its effects by binding to GABA-A receptors, which are ligand-gated chloride channels. When GABA binds to these receptors, it opens the chloride channel, leading to an influx of chloride ions into the neuron and hyperpolarization of the membrane, making it less likely to fire.

GABA-A receptor antagonists work by binding to the GABA-A receptor and preventing GABA from binding, thereby blocking the inhibitory effects of GABA. This can lead to increased neuronal excitability and can result in a variety of effects depending on the specific antagonist and the location of the receptors involved.

GABA-A receptor antagonists have been used in research to study the role of GABA in various physiological processes, and some have been investigated as potential therapeutic agents for conditions such as anxiety, depression, and insomnia. However, their use is limited by their potential to cause seizures and other adverse effects due to excessive neuronal excitation. Examples of GABA-A receptor antagonists include picrotoxin, bicuculline, and flumazenil.

Anti-anxiety agents, also known as anxiolytics, are a class of medications used to manage symptoms of anxiety disorders. These drugs work by reducing the abnormal excitement in the brain and promoting relaxation and calmness. They include several types of medications such as benzodiazepines, azapirone, antihistamines, and beta-blockers.

Benzodiazepines are the most commonly prescribed anti-anxiety agents. They work by enhancing the inhibitory effects of a neurotransmitter called gamma-aminobutyric acid (GABA) in the brain, which results in sedative, hypnotic, anxiolytic, anticonvulsant, and muscle relaxant properties. Examples of benzodiazepines include diazepam (Valium), alprazolam (Xanax), lorazepam (Ativan), and clonazepam (Klonopin).

Azapirones are a newer class of anti-anxiety agents that act on serotonin receptors in the brain. Buspirone (Buspar) is an example of this type of medication, which has fewer side effects and less potential for abuse compared to benzodiazepines.

Antihistamines are medications that are primarily used to treat allergies but can also have anti-anxiety effects due to their sedative properties. Examples include hydroxyzine (Vistaril, Atarax) and diphenhydramine (Benadryl).

Beta-blockers are mainly used to treat high blood pressure and heart conditions but can also help manage symptoms of anxiety such as rapid heartbeat, tremors, and sweating. Propranolol (Inderal) is an example of a beta-blocker used for this purpose.

It's important to note that anti-anxiety agents should be used under the guidance of a healthcare professional, as they can have side effects and potential for dependence or addiction. Additionally, these medications are often used in combination with psychotherapy and lifestyle modifications to manage anxiety disorders effectively.

Conscious sedation, also known as procedural sedation and analgesia, is a minimally depressed level of consciousness that retains the patient's ability to maintain airway spontaneously and respond appropriately to physical stimulation and verbal commands. It is typically achieved through the administration of sedative and/or analgesic medications and is commonly used in medical procedures that do not require general anesthesia. The goal of conscious sedation is to provide a comfortable and anxiety-free experience for the patient while ensuring their safety throughout the procedure.

Triazolam is a short-acting benzodiazepine drug, which is primarily used for the treatment of insomnia. It works by increasing the activity of gamma-aminobutyric acid (GABA), a neurotransmitter that inhibits the activity of neurons in the brain, thereby producing a calming effect. Triazolam has a rapid onset of action and its effects typically last for 1-2 hours, making it useful for inducing sleep. However, due to its short duration of action and potential for dependence and tolerance, triazolam is generally recommended for short-term use only.

Like all benzodiazepines, triazolam carries a risk of serious side effects, including respiratory depression, physical dependence, and cognitive impairment. It should be used with caution and under the close supervision of a healthcare provider.

Carbolines are a type of chemical compound that contain a carbazole or dibenzopyrrole structure. These compounds have a variety of uses, including as pharmaceuticals and dyes. Some carbolines have been studied for their potential medicinal properties, such as their ability to act as antioxidants or to inhibit the growth of certain types of cells. However, it is important to note that many carbolines are also known to be toxic and can cause harm if ingested or otherwise introduced into the body. As with any chemical compound, it is essential to use caution when handling carbolines and to follow all safety guidelines to minimize the risk of exposure.

Dental anesthesia is a type of local or regional anesthesia that is specifically used in dental procedures to block the transmission of pain impulses from the teeth and surrounding tissues to the brain. The most common types of dental anesthesia include:

1. Local anesthesia: This involves the injection of a local anesthetic drug, such as lidocaine or prilocaine, into the gum tissue near the tooth that is being treated. This numbs the area and prevents the patient from feeling pain during the procedure.
2. Conscious sedation: This is a type of minimal sedation that is used to help patients relax during dental procedures. The patient remains conscious and can communicate with the dentist, but may not remember the details of the procedure. Common methods of conscious sedation include nitrous oxide (laughing gas) or oral sedatives.
3. Deep sedation or general anesthesia: This is rarely used in dental procedures, but may be necessary for patients who are extremely anxious or have special needs. It involves the administration of drugs that cause a state of unconsciousness and prevent the patient from feeling pain during the procedure.

Dental anesthesia is generally safe when administered by a qualified dentist or oral surgeon. However, as with any medical procedure, there are risks involved, including allergic reactions to the anesthetic drugs, nerve damage, and infection. Patients should discuss any concerns they have with their dentist before undergoing dental anesthesia.

GABA-A receptor agonists are substances that bind to and activate GABA-A receptors, which are ligand-gated ion channels found in the central nervous system. GABA (gamma-aminobutyric acid) is the primary inhibitory neurotransmitter in the brain, and its activation via GABA-A receptors results in hyperpolarization of neurons and reduced neuronal excitability.

GABA-A receptor agonists can be classified into two categories: GABAergic compounds and non-GABAergic compounds. GABAergic compounds, such as muscimol and isoguvacine, are structurally similar to GABA and directly activate the receptors. Non-GABAergic compounds, on the other hand, include benzodiazepines, barbiturates, and neurosteroids, which allosterically modulate the receptor's affinity for GABA, thereby enhancing its inhibitory effects.

These agents are used in various clinical settings to treat conditions such as anxiety, insomnia, seizures, and muscle spasticity. However, they can also produce adverse effects, including sedation, cognitive impairment, respiratory depression, and physical dependence, particularly when used at high doses or for prolonged periods.

Chlordiazepoxide is a medication that belongs to a class of drugs known as benzodiazepines. It is primarily used to treat anxiety disorders, but can also be used for the short-term relief of symptoms related to alcohol withdrawal and muscle spasms. Chlordiazepoxide works by enhancing the activity of gamma-aminobutyric acid (GABA), a neurotransmitter that inhibits nerve impulses in the brain, resulting in sedative, hypnotic, anxiolytic, anticonvulsant, and muscle relaxant properties.

The medication is available in both immediate-release and extended-release forms, and is typically taken orally. Common side effects of chlordiazepoxide include dizziness, drowsiness, and impaired coordination. More serious side effects can include memory problems, confusion, and difficulty breathing. Chlordiazepoxide can also be habit-forming, so it is important to use the medication only as directed by a healthcare provider.

It's important to note that chlordiazepoxide can interact with other medications, including certain antidepressants, opioids, and sedatives, so it's essential to inform your doctor about all the medications you are taking before starting chlordiazepoxide. Additionally, this medication should not be used during pregnancy or while breastfeeding, as it can cause harm to the developing fetus or newborn baby.

Delayed emergence from anesthesia is a medical condition where a patient takes an unusually long time to regain consciousness after general anesthesia. The exact duration of "normal" emergence can vary depending on several factors, including the type and duration of anesthesia, the patient's age, health status, and other medications they may be taking. However, if a patient has not regained full consciousness within 30 minutes to an hour after the surgery, it is generally considered a delayed emergence.

There can be various causes for delayed emergence from anesthesia. Some of the common reasons include:

1. Residual effects of anesthetic drugs: If the anesthesiologist has not adequately reversed the muscle relaxants or if the anesthetic agents have a prolonged action, it can delay the patient's emergence from anesthesia.
2. Hypothermia: Accidental hypothermia during surgery can slow down the metabolism of anesthetic drugs and contribute to delayed emergence.
3. Hypoventilation or hypercarbia: Inadequate ventilation leading to high carbon dioxide levels in the blood can prolong recovery from anesthesia.
4. Metabolic or endocrine disorders: Conditions such as diabetes, hypothyroidism, or electrolyte imbalances can affect the patient's response to anesthesia and delay emergence.
5. Postoperative complications: Complications like stroke, heart attack, or bleeding can also cause delayed emergence from anesthesia.
6. Medications: Certain medications, such as sedatives or opioids, can interact with anesthetic drugs and prolong recovery.
7. Patient factors: Older age, poor health status, and certain genetic factors can contribute to a delayed emergence from anesthesia.

Anesthesiologists closely monitor patients during the recovery phase and take appropriate measures to address any potential causes of delayed emergence. This may include providing additional oxygen, adjusting ventilation, administering reversal agents for muscle relaxants, or addressing any underlying medical conditions. In some cases, further evaluation in an intensive care unit (ICU) might be necessary to ensure the patient's safety and proper recovery.

The anesthesia recovery period, also known as the post-anesthetic care unit (PACU) or recovery room stay, is the time immediately following anesthesia and surgery during which a patient's vital signs are closely monitored as they emerge from the effects of anesthesia.

During this period, the patient is typically observed for adequate ventilation, oxygenation, circulation, level of consciousness, pain control, and any potential complications. The length of stay in the recovery room can vary depending on the type of surgery, the anesthetic used, and the individual patient's needs.

The anesthesia recovery period is a critical time for ensuring patient safety and comfort as they transition from the surgical setting to full recovery. Nurses and other healthcare providers in the recovery room are specially trained to monitor and manage patients during this vulnerable period.

Hypnotics and sedatives are classes of medications that have depressant effects on the central nervous system, leading to sedation (calming or inducing sleep), reduction in anxiety, and in some cases, decreased awareness or memory. These agents work by affecting the neurotransmitter GABA (gamma-aminobutyric acid) in the brain, which results in inhibitory effects on neuronal activity.

Hypnotics are primarily used for the treatment of insomnia and other sleep disorders, while sedatives are often prescribed to manage anxiety or to produce a calming effect before medical procedures. Some medications can function as both hypnotics and sedatives, depending on the dosage and specific formulation. Common examples of these medications include benzodiazepines (such as diazepam and lorazepam), non-benzodiazepine hypnotics (such as zolpidem and eszopiclone), barbiturates, and certain antihistamines.

It is essential to use these medications under the guidance of a healthcare professional, as they can have potential side effects, such as drowsiness, dizziness, confusion, and impaired coordination. Additionally, long-term use or high doses may lead to tolerance, dependence, and withdrawal symptoms upon discontinuation.

Zolazepam is a veterinary medication that belongs to a class of drugs called benzodiazepines. It is used in the induction and maintenance of anesthesia in animals, often in combination with other medications. Zolazepam works by depressing the central nervous system, producing sedation, muscle relaxation, and amnesia.

In veterinary medicine, zolazepam is commonly combined with tiletamine, another dissociative anesthetic, to form a drug called Telazol. This combination provides balanced anesthesia with minimal cardiovascular and respiratory depression.

It's important to note that zolazepam is not approved for use in humans and should only be administered by trained veterinary professionals under strict supervision.

Flunitrazepam is a benzodiazepine drug, which has sedative, hypnotic, muscle relaxant, and anticonvulsant properties. Its primary use is for the treatment of severe insomnia and occasionally for managing anxiety disorders. It works by enhancing the effects of gamma-aminobutyric acid (GABA), a neurotransmitter in the brain that inhibits the activity of nerve cells and produces a calming effect.

Flunitrazepam is also known by its brand name, Rohypnol, and has gained notoriety for its use as a date-rape drug due to its ability to cause sedation, amnesia, and muscle relaxation at high doses. It is important to note that flunitrazepam is a controlled substance in many countries and its use without a prescription is illegal.

Tiletamine is a veterinary medication that belongs to the class of drugs known as dissociative anesthetics. It is often used in combination with zolazepam, and the combination is sold under the brand name Telazol. This drug combination is primarily used for the induction and maintenance of anesthesia in various animal species.

Tiletamine works by blocking the action of N-methyl-D-aspartate (NMDA) receptors, which are involved in pain perception, learning, and memory. By doing so, it produces a state of dissociation, where animals may appear to be conscious but are not aware of their surroundings or the procedures being performed on them.

It is important to note that tiletamine should only be used under the direction of a licensed veterinarian, as its use requires proper training and experience to ensure safe and effective administration.

Lorazepam is a medication that belongs to a class of drugs known as benzodiazepines. Medically, it is defined as a prescription drug used for the treatment of anxiety disorders, short-term relief of symptoms of anxiety or anxiety associated with depressive symptoms. It can also be used for the treatment of insomnia, seizure disorders, and alcohol withdrawal. Lorazepam works by affecting chemicals in the brain that may become unbalanced and cause anxiety or other symptoms.

It is important to note that lorazepam can be habit-forming and should only be used under the supervision of a healthcare provider. Misuse of this medication can lead to serious risks, including addiction, overdose, or death.

Pregnenolone is defined as a neurosteroid, which is a steroid hormone that is produced in the nervous system. It is synthesized from cholesterol and is the precursor to other steroid hormones, including progesterone, cortisol, and the sex hormones (estrogens and androgens). Pregnenolone has been shown to have a number of important functions in the body, including modulation of neurotransmitter systems, regulation of ion channels, and protection of nerve cells from damage. It is thought to play a role in various physiological processes, such as memory, learning, and mood regulation. However, more research is needed to fully understand its mechanisms of action and therapeutic potential.

Sodium oxybate is a central nervous system depressant, which is a sodium salt of gamma-hydroxybutyric acid (GHB). It is also known as gamma-hydroxybutyrate monosodium salt or sodium GHB. Sodium oxybate is used in the medical field for the treatment of narcolepsy, a sleep disorder characterized by excessive daytime sleepiness and cataplexy (sudden loss of muscle tone). It is sold under the brand name Xyrem.

Sodium oxybate works by affecting the neurotransmitters in the brain, specifically increasing the levels of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter that helps regulate sleep and wakefulness. The medication is available only through a restricted distribution program due to its potential for abuse and dependence. It is usually taken at night in two doses, one at bedtime and the other about 2.5 to 4 hours later.

It's important to note that sodium oxybate has a high potential for misuse and addiction, and it should only be used under the close supervision of a healthcare provider.

Carbon radioisotopes are radioactive isotopes of carbon, which is an naturally occurring chemical element with the atomic number 6. The most common and stable isotope of carbon is carbon-12 (^12C), but there are also several radioactive isotopes, including carbon-11 (^11C), carbon-14 (^14C), and carbon-13 (^13C). These radioisotopes have different numbers of neutrons in their nuclei, which makes them unstable and causes them to emit radiation.

Carbon-11 has a half-life of about 20 minutes and is used in medical imaging techniques such as positron emission tomography (PET) scans. It is produced by bombarding nitrogen-14 with protons in a cyclotron.

Carbon-14, also known as radiocarbon, has a half-life of about 5730 years and is used in archaeology and geology to date organic materials. It is produced naturally in the atmosphere by cosmic rays.

Carbon-13 is stable and has a natural abundance of about 1.1% in carbon. It is not radioactive, but it can be used as a tracer in medical research and in the study of metabolic processes.

Benzodiazepines are a class of psychoactive drugs that possess anxiolytic, anticonvulsant, amnesic, sedative, hypnotic, and muscle relaxant properties. Benzodiazepinones are a subclass of benzodiazepines that share a specific chemical structure, characterized by a 1,4-benzodiazepine ring with an additional nitrogen-containing ring attached at the 2-position of the benzodiazepine ring.

Examples of benzodiazepinones include clonazepam (Klonopin), diazepam (Valium), and flurazepam (Dalmane). These medications are commonly used in the treatment of anxiety disorders, insomnia, seizures, and muscle spasms. However, they can also cause physical dependence and withdrawal symptoms, so they should be prescribed with caution and under medical supervision.

A coma is a deep state of unconsciousness in which an individual cannot be awakened, cannot respond to stimuli, and does not exhibit any sleep-wake cycles. It is typically caused by severe brain injury, illness, or toxic exposure that impairs the function of the brainstem and cerebral cortex.

In a coma, the person may appear to be asleep, but they are not aware of their surroundings or able to communicate or respond to stimuli. Comas can last for varying lengths of time, from days to weeks or even months, and some people may emerge from a coma with varying degrees of brain function and disability.

Medical professionals use various diagnostic tools and assessments to evaluate the level of consciousness and brain function in individuals who are in a coma, including the Glasgow Coma Scale (GCS), which measures eye opening, verbal response, and motor response. Treatment for coma typically involves supportive care to maintain vital functions, manage any underlying medical conditions, and prevent further complications.

Doxapram is a central stimulant drug that acts on the respiratory system. It is primarily used to stimulate breathing and promote wakefulness in patients who have reduced levels of consciousness or are experiencing respiratory depression due to various causes, such as anesthesia or medication overdose.

Doxapram works by stimulating the respiratory center in the brainstem, increasing the rate and depth of breathing. It also has a mild stimulant effect on the central nervous system, which can help to promote wakefulness and alertness.

The drug is available in various forms, including injectable solutions and inhaled powders. It is typically administered under medical supervision in a hospital or clinical setting due to its potential for causing adverse effects such as agitation, anxiety, and increased heart rate and blood pressure.

It's important to note that doxapram should only be used under the direction of a healthcare professional, as improper use can lead to serious complications.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

GABA (gamma-aminobutyric acid) agonists are substances that bind to and activate GABA receptors in the brain, mimicking the actions of GABA, which is the primary inhibitory neurotransmitter in the central nervous system. These agents can produce various effects such as sedation, anxiolysis, muscle relaxation, and anticonvulsant activity by enhancing the inhibitory tone in the brain. They are used clinically to treat conditions such as anxiety disorders, seizures, and muscle spasticity. Examples of GABA agonists include benzodiazepines, barbiturates, and certain non-benzodiazepine hypnotics.

Emission computed tomography (ECT) is a type of tomographic imaging technique in which an emission signal from within the body is detected to create cross-sectional images of that signal's distribution. In Emission-Computed Tomography (ECT), a radionuclide is introduced into the body, usually through injection, inhalation or ingestion. The radionuclide emits gamma rays that are then detected by external gamma cameras.

The data collected from these cameras is then used to create cross-sectional images of the distribution of the radiopharmaceutical within the body. This allows for the identification and quantification of functional information about specific organs or systems within the body, such as blood flow, metabolic activity, or receptor density.

One common type of Emission-Computed Tomography is Single Photon Emission Computed Tomography (SPECT), which uses a single gamma camera that rotates around the patient to collect data from multiple angles. Another type is Positron Emission Tomography (PET), which uses positron-emitting radionuclides and detects the coincident gamma rays emitted by the annihilation of positrons and electrons.

Overall, ECT is a valuable tool in medical imaging for diagnosing and monitoring various diseases, including cancer, heart disease, and neurological disorders.

Substance Withdrawal Syndrome is a medically recognized condition that occurs when an individual who has been using certain substances, such as alcohol, opioids, or benzodiazepines, suddenly stops or significantly reduces their use. The syndrome is characterized by a specific set of symptoms that can be physical, cognitive, and emotional in nature. These symptoms can vary widely depending on the substance that was being used, the length and intensity of the addiction, and individual factors such as genetics, age, and overall health.

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), published by the American Psychiatric Association, provides the following diagnostic criteria for Substance Withdrawal Syndrome:

A. The development of objective evidence of withdrawal, referring to the specific physiological changes associated with the particular substance, or subjective evidence of withdrawal, characterized by the individual's report of symptoms that correspond to the typical withdrawal syndrome for the substance.

B. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

C. The symptoms are not better explained by co-occurring mental, medical, or other substance use disorders.

D. The withdrawal syndrome is not attributable to another medical condition and is not better accounted for by another mental disorder.

The DSM-5 also specifies that the diagnosis of Substance Withdrawal Syndrome should be substance-specific, meaning that it should specify the particular class of substances (e.g., alcohol, opioids, benzodiazepines) responsible for the withdrawal symptoms. This is important because different substances have distinct withdrawal syndromes and require different approaches to management and treatment.

In general, Substance Withdrawal Syndrome can be a challenging and potentially dangerous condition that requires professional medical supervision and support during the detoxification process. The specific symptoms and their severity will vary depending on the substance involved, but they may include:

* For alcohol: tremors, seizures, hallucinations, agitation, anxiety, nausea, vomiting, and insomnia.
* For opioids: muscle aches, restlessness, lacrimation (tearing), rhinorrhea (runny nose), yawning, perspiration, chills, mydriasis (dilated pupils), piloerection (goosebumps), nausea or vomiting, diarrhea, and abdominal cramps.
* For benzodiazepines: anxiety, irritability, insomnia, restlessness, confusion, hallucinations, seizures, and increased heart rate and blood pressure.

It is essential to consult with a healthcare professional if you or someone you know is experiencing symptoms of Substance Withdrawal Syndrome. They can provide appropriate medical care, support, and referrals for further treatment as needed.

Pentylenetetrazole (PTZ) is not primarily considered a medical treatment, but rather a research compound used in neuroscience and neurology to study seizure activity and chemically induce seizures in animals for experimental purposes. It is classified as a proconvulsant agent. Medically, it has been used in the past as a medication to treat epilepsy, but its use is now largely historical due to the availability of safer and more effective anticonvulsant drugs.

In a medical or scientific context, Pentylenetetrazole can be defined as:

A chemical compound with the formula C6H5N5O2, which is used in research to investigate seizure activity and induce convulsions in animals. It acts as a non-competitive GABAA receptor antagonist and can lower the seizure threshold. Historically, it has been used as a medication to treat epilepsy, but its use for this purpose is now limited due to the development of safer and more effective anticonvulsant drugs.

Flumazenil (also known as flumazepil, code name Ro 15-1788) is a selective GABAA receptor antagonist administered via injection ... Administration of flumazenil by sublingual lozenge and topical cream has also been tested. Flumazenil benefits patients who ... Romazicon product information, Roche USA Media related to Flumazenil at Wikimedia Commons Flumazenil drug label/data at ... slowly infused flumazenil. One addiction treatment centre in Italy has used flumazenil to treat over 300 patients who were ...
Flumazenil injection is indicated for a complete or partial reversal of the sedative effects of benzodiazepines in conscious ... The primary FDA-approved clinical uses for flumazenil include reversal agents for benzodiazepine overdose and postoperative ... and toxicity of flumazenil so that providers can direct patient therapy to optimal outcomes in benzodiazepine reversal. ... The Flumazenil Pediatric Study Group.[J Pediatr. 1997]. Safety and efficacy of flumazenil in the reversal of benzodiazepine- ...
FLUMAZENIL (UNII: 40P7XK9392) (FLUMAZENIL - UNII:40P7XK9392) FLUMAZENIL. 0.1 mg in 1 mL. ... FLUMAZENIL (UNII: 40P7XK9392) (FLUMAZENIL - UNII:40P7XK9392) FLUMAZENIL. 0.1 mg in 1 mL. ... Flumazenil injection is contraindicated:. •. in patients with a known hypersensitivity to flumazenil or benzodiazepines.. •. in ... Flumazenil should be used in such settings with extreme caution, since the use of flumazenil in this situation has not been ...
... Pharmacol Ther. 1990;45(3):331-43. doi: 10.1016/0163-7258(90) ...
Flumazenil is used to help you wake up after a surgery or medical procedure in which a benzodiazepine was used as a sedative. ... Flumazenil is used to reverse the effects of a benzodiazepine (BENZ-oh-dye-AYZ-e-peen) sedative such as Valium, Versed, Xanax, ... What is flumazenil? What is flumazenil?. Flumazenil is used to reverse the effects of a benzodiazepine (BENZ-oh-dye-AYZ-e-peen ... How is flumazenil given? How is flumazenil given?. Flumazenil is given as an infusion into a vein. A healthcare provider will ...
On this page about Flumazenil (Apotex) you will find information relating to side effects, age restrictions, food interactions ... Brand name: Flumazenil (Apotex) TM. Active ingredients: flumazenil On December 1, 2023 Flumazenil (Apotex) was not listed on ... Other medicines containing the same active ingredients: flumazenil *Can I take Flumazenil (Apotex) in sport? Find out on the ...
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Flumazenil [CAS Number 78755-81-4] Flumazenil is a selective GABAA receptor antagonist and benzodiazepine derivative primarily ... Flumazenil. Product reference number. FLM-115. Full chemical name. Ethyl 8-fluoro-5-methyl-5,6-dihydro-6-oxo-4H-imidazo(1,5-a)( ... BeschreibungFlumazenil Product reference number FLM-115 Full chemical name Ethyl 8-fluoro-5-methyl-5,6-dihydro-6-oxo-4H-imidazo ... Flumazenil is available as reference material (bulk powder and/or solution) and as calibrated, Ready-to-Use, certified ...
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Flumazenil. Flumazenil is a competitive antagonist of the benzodiazepine class of drugs. The onset of action is within 1-2 ... Flumazenil is generally given in increments of 0.2 mg, titrated to effect. In pediatrics, the dose is 0.01 mg/kg, up to 0.2 mg ...
Flumazenil (Mazicon) answers are found in the Clinical Anesthesia Procedures powered by Unbound Medicine. Available for iPhone ... "Flumazenil (Mazicon)." Clinical Anesthesia Procedures, 9th ed., Wolters Kluwer, 2019. Anesthesia Central, anesth. ... unboundmedicine.com/anesthesia/view/ClinicalAnesthesiaProcedures/728047/all/Flumazenil__Mazicon_. Flumazenil (Mazicon). In: ... Flumazenil (Mazicon) [Internet]. In: Pino RMR, editors. Clinical Anesthesia Procedures. Wolters Kluwer; 2019. [cited 2023 ...
Flumazenil is short acting, with a half-life of 0.7-1.3 hours. However, because most benzodiazepines have longer half-lives, ... Flumazenil reverses the effects of benzodiazepines in an overdose by selectively antagonizing the gamma-aminobutyric acid (GABA ...
Ultimately, flumazenil 0.5mg was given in divided doses to reverse the effects of midazolam. Within three minutes the patient ... We report a case in which a postoperative paradoxical reaction to midazolam was successfully managed with flumazenil (a ... Thurston TA, Williams CGA (1996) Reversal of a paradoxical reaction to midazolam with flumazenil. Anesthesia and Analgesia 83: ... demonstrate even small amounts of flumazenil can be effective in treating this. Despite the risks associated with the use of ...
Flumazenils duration of action is 1 hour and may wear off before the benzodiazepine. Therefore, patients treated with ... If respiration is compromised, assist with breathing (airway management, oxygen and ambu bag) and reverse with flumazenil (see ... If respiration is compromised, assist with breathing (airway management, oxygen and ambu bag) and reverse with flumazenil (see ... If respiration is compromised, assist with breathing (airway management, oxygen and ambu bag) and reverse with flumazenil (see ...
We conclude that neither potentiation of GABA transmission (midazolam) nor antagonism of this potentiation (flumazenil) greatly ... during infusion of flumazenil (a benzodiazepine antagonist). On each experimental day, the following protocol was repeated ... Effects of midazolam and flumazenil on ventilation during sustained hypoxia in humans. ... We conclude that neither potentiation of GABA transmission (midazolam) nor antagonism of this potentiation (flumazenil) greatly ...
N2 - Previous [11C]flumazenil (FMZ) positron emission tomography (PET) investigations in patients with idiopathic generalized ... AB - Previous [11C]flumazenil (FMZ) positron emission tomography (PET) investigations in patients with idiopathic generalized ... Previous [11C]flumazenil (FMZ) positron emission tomography (PET) investigations in patients with idiopathic generalized ... abstract = "Previous [11C]flumazenil (FMZ) positron emission tomography (PET) investigations in patients with idiopathic ...
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Flumazenil 100 micrograms/ml Solution for injection/infusion. (0.5 mg in 5 ml) For further information on this product please ... Flumazenil 100 micrograms/ml 0.5 mg in 5 ml. 10 x 5 ml AMP. ...
3. Flumazenil. Some studies have found that low doses of Flumazenil, a drug often used in cases of benzodiazepine overdose, can ...
The Interactions of Midazolam and Flumazenil on Human Memory and Cognition M. M. Ghoneim, M.D.; M. M. Ghoneim, M.D. ... Effect of Flumazenil on Ventilatory Drive during Sedation with Midazolam and Alfentanil Anesthesiology (October 1996) ... Flumazenil Mimics whereas Midazolam Abolishes Ischemic Preconditioning in a Rabbit Heart Model of Ischemia-Reperfusion ... Effect of Flumazenil on Bispectral Index Monitoring in Unpremedicated Patients Anesthesiology (May 2009) ...
Detailed drug Information for Limbitrol. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
Procainamide reference guide for safe and effective use from the American Society of Health-System Pharmacists (AHFS DI).
... and flumazenil (Flu) on stress-related neurohormonal and metabolic responses in isoflurane-anesthetized cats premedicated with ... This study examined the post-operative effects of atipamezole (Ati) and flumazenil (Flu) on stress-related neurohormonal and ... Effects of atipamezole and flumazenil on stress-related hormonal and metabolic responses in cats anesthetized with medetomidine ... Kamohara, Hirokazu; Kamohara, Toshiko; and Hikasa, Yoshiaki (2022) "Effects of atipamezole and flumazenil on stress-related ...
Neurocognitive performance, alcohol withdrawal, and effects of a combination of flumazenil and gabapentin in alcohol dependence ... Neurocognitive performance, alcohol withdrawal, and effects of a combination of flumazenil and gabapentin in alcohol dependence ... Neurocognitive performance, alcohol withdrawal, and effects of a combination of flumazenil and gabapentin in alcohol dependence ...
Comparison of the recovery profile of remimazolam with flumazenil and propofol anesthesia for open thyroidectomy Previous ... reported a slower recovery of consciousness following remimazolam-based total intravenous anesthesia without flumazenil than ...
Masui K. Caution!! Reappearance of remimazolam effect after a flumazenil bolus: a larger bolus of flumazenil and a lower total ... Considering the half-life of flumazenil, it has been noted that resedation even after administration of flumazenil can occur in ... Araki, H., Inoue, S. Switching to remimazolam followed by flumazenil may be a promising combination for deep extubation. JA ... Switching to remimazolam followed by flumazenil may be a promising combination for deep extubation. *Hideharu Araki1 & ...
May interact with flumazenil [43].. Main side effects :. General: nausea, vomiting, tachycardia, hypertension, postoperative ...

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