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Selective serotonin receptor inhibitor SSRI

Pharmacological treatment of OSA is an elusive concept. A number of selective serotonin receptor inhibitors (SSRIs) and other medications were tried and found to be ineffective. SSRIs and analogous medication have been anecdotally reported to help REM-related OSA, but no study systematically confirmed this claim. Two studies showed positive effect of mirtazapine [33, 34], a tetracyclic non-SSRI antidepressant, on OSA, but further research on a bigger sample is necessary. On the other hand, one should be aware of a muscle relaxation property of some commonly used medications such as benzodiazepines (BZDs), which may result in a worsening of OSA. Assisted nasal ventilation is commonly used in patients with both hypercapnic and non-hypercapnic CSA. The administration of oxygen is observed to ameliorate the frequency of both the central and obstructive events in patients with a predomi-... [Pg.159]

With respect to a specific and common clinical problem, advice to withdraw hypnotic medication should follow a careful evaluation of self-reported sleep patterns, psychological factors and psychosocial status. Ambulant monitoring can be helpful in patients who have encountered severe problems in effecting withdrawal. A careful psychiatric assessment should be made to ascertain whether the patient has clinically significant anxiety and/or depression. Both should be treated with a selective serotonin receptor inhibitor (SSRI) before withdrawal from the hypnotic is attempted. An optimal tapering schedule should be discussed with the patient some will attempt a rapid withdrawal over less than 8 weeks and others will require much longer. This is particularly so if previous attempts to withdraw have been unsuccessful. Carers, family and friends should be mobilized to help in withdrawal, should the patient wish this. Substitution of zolpidem may facilitate withdrawal but should be kept as a reserve strategy. [Pg.257]

Dexamethasone has been nsed successfully in the management of chemotherapy-indnced and postoperative nansea and vomiting, either as a single agent or in combination with selective serotonin receptor inhibitors (SSRIs). For chemotherapy-indnced nansea and vomiting, dexamethasone has demonstrated efficacy in the prevention of both cisplatin-indnced acnte emesis" and delayed nansea and... [Pg.670]

Beginning in the 1960s, ben2odia2epiae anxiolytics and hypnotics rapidly became the standard prescription dmg treatment. In the 1980s, buspkone [36505-84-7] (3), which acts as a partial agonist at the serotonin [50-67-9] (5-hydroxytryptamine, 5-HT) type lA receptor, was approved as treatment for generali2ed anxiety. More recently, selective serotonin reuptake inhibitors (SSRIs) have been approved for therapy of panic disorder and obsessive—compulsive behavior. [Pg.218]

Recent evidence indicates that the 5-HT transporter is subject to post-translational regulatory changes in much the same way as neurotransmitter receptors (Blakeley et al. 1998). Protein kinase A and protein kinase C (PKC), at least, are known to be involved in this process. Phosphorylation of the transporter by PKC reduces the Fmax for 5-HT uptake and leads to sequestration of the transporter into the cell, suggesting that this enzyme has a key role in its intracellular trafficking. Since this phosphorylation is reduced when substrates that are themselves transported across the membrane bind to the transporter (e.g. 5-HT and fi -amphetamine), it seems that the transport of 5-HT is itself linked with the phosphorylation process. Possibly, this process serves as a homeostatic mechanism which ensures that the supply of functional transporters matches the demand for transmitter uptake. By contrast, ligands that are not transported (e.g. cocaine and the selective serotonin reuptake inhibitors (SSRIs)) prevent the inhibition of phosphorylation by transported ligands. Thus, such inhibitors would reduce 5-HT uptake both by their direct inhibition of the transporter and by disinhibition of its phosphorylation (Ramamoorthy and Blakely 1999). [Pg.195]

FDA, Combined Use of 5-Hydroxytryptamine Receptor Agonists (Triptans), Selective Serotonin Reuptake Inhibitors (SSRIs) or Selective Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs) May Result in Life-Threatening Serotonin Syndrome , FDA Public Health Advisory (2006) http //www.fda.gov/Cder/Drug/advisory/ S SRI S S200607.htm... [Pg.201]

The most commonly used therapies for anxiety and depression are selective serotonin reuptake inhibitors (SSRIs) and the more recently developed serotonin noradrenaline reuptake inhibitors (SNRIs). SSRIs, which constitute 60% of the worldwide antidepressant and antianxiety market, are frequently associated with sexual dysfunction, appetite disturbances and sleep disorders. Because SSRIs and SNRIs increase 5-HT levels in the brain, they can indirectly stimulate all 14 serotonergic receptor subtypes [2,3], some of which are believed to lead to adverse side effects associated with these drugs. Common drugs for short-term relief of GAD are benzodiazepines. These sedating agents are controlled substances with addictive properties and can be lethal when used in combination with alcohol. The use of benzodiazepines is associated with addiction, dependency and cognitive impairment. [Pg.458]

A life-threatening condition, when selective serotonin reuptake inhibitors (SSRIs) and 5-hydroxytryptamine receptor agonists (triptans) are used together. However, many other drugs have been implicated (see below). Signs and symptoms of serotonin syndrome include the following ... [Pg.357]

Trazodone (Apothecon) is also classified as an antidepressant agent. It is a selective serotonin reuptake inhibitor (SSRI), partial agonist at postsynaptic 5-HTia receptors, and exhibits a-adrenoceptor blocking actions. [Pg.739]

The selective serotonin reuptake inhibitors (SSRIs) represent a chemically diverse class of agents that have as their primary action the inhibition of the serotonin transporter (SERT) (Figure 30-3). Fluoxetine was introduced in the United States in 1988 and quickly became one of the most commonly prescribed medications in medical practice. The development of fluoxetine emerged out of the search for chemicals that had high affinity for monoamine receptors but lacked the affinity for histamine, acetylcholine, and adrenoceptors that is seen with the tricyclic antidepressants (TCAs). There are currently six available SSRIs, and they are the most common antidepressants in clinical use. In addition to their use in major depression, SSRIs have indications in GAD, PTSD, OCD, panic disorder, PMDD, and bulimia. Fluoxetine, sertraline, and citalopram exist as isomers and are formulated in the racemic forms, whereas paroxetine and fluvoxamine are not optically active. Escitalopram is the S enantiomer of citalopram. As with all antidepressants,... [Pg.652]

Selective serotonin reuptake inhibitors (SSRIs) promote sleep by inhibiting uptake of serotonin. They vary widely in their propensity to cause sleep onset delay and sleep disruption (e.g., fluoxetine) and sedation (citralopram). Trazadone, a 5HT agonist, is a more powerful sedating agent because it inhibits binding of serotonin and blocks histamine receptors, thus sedating via two mechanisms. SSRIs may exacerbate preexisting RLS and PLMs. [Pg.143]


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See also in sourсe #XX -- [ Pg.87 , Pg.88 , Pg.231 ]




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Inhibitors selection

Receptor inhibitors

SSRIs

SSRIs inhibitors

Selective inhibitor

Selective receptors

Selective serotonin

Selective serotonin inhibitors

Serotonin inhibitors

Serotonin receptor

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