Drugs online research references
Acad Emerg Med. 1996 Feb;3(2):132-6.
Sertraline overdose.
Lau GT, Horowitz BZ.
Division of Emergency Medicine and Clinical Toxicology, University of California, Davis, Medical Center, Sacramento 95817, USA.
OBJECTIVE: To determine the clinical presenting signs and symptoms in presumed overdoses of sertraline, a recently approved antidepressant. METHODS: A prospective study involving five western regional poison control centers was performed to evaluate the clinical manifestations of presumed sertraline ingestions (overdoses). Information about calls pertaining to sertraline ingestions was recorded on a standard data collection form. Data including subject age, sex, amount ingested, coingestants, time interval to evaluation, vital signs, presenting signs and symptoms, ECG abnormalities, treatment given, disposition, and length of stay in the ED were collected over a nine-month period. RESULTS: Of 42 ingestions reported, two were adverse reactions to normal doses and 40 were overdoses. Stated amounts of sertraline ingested ranged from 50 to 8,000 mg (mean 1,579 mg). Mean patient age was 35.3 years (range 1 to 69 years). Mean interval to presentation was 3.0 hours. Seventeen of the 40 patients ingested sertraline alone. Of this subgroup, ten had no sign or symptom. The most common abnormalties reported in isolated sertraline overdose were tremor, lethargy, and nausea. Less common findings included agitation, confusion, and vomiting. There was no significant morbidity in this subgroup of presumed isolated sertraline ingestion. Of the 23 patients who ingested other medications along with sertraline, four were asymptomatic. Benzodiazepines and alcohol were the most frequently coingested substances. Lethargy, nausea, dry mouth, and mydriasis were the most common features reported in this group. Treatment included lavage, activated charcoal, and observation. Twelve patients were admitted for 24-hour observation, none had an adverse outcome. Of the patients released from the ED, the mean length of stay was 3.9 hours. CONCLUSION: Sertraline is commonly taken in overdose with other medications or alcohol. The signs and symptoms that develop in association with an overdose of sertraline appear to be minor and of short duration.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8808373&dopt=Abstract
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Life Sci. 1996;59(14):1109-19.
Differential potentiation of L-tryptophan-induced head-twitch response in mice by cocaine and sertraline.
Darmani NA.
Department of Pharmacology Kirksville College of Osteopathic Medicine, MO 63501, USA.
Using selective monoamine uptake blockers and appropriate selective monoamine receptor antagonists, we have previously shown that cocaine enhances the frequency of 5-HT2A receptor-mediated 5-hydroxytryptophan (5-HTP)-induced head-twitch response (HTR) in mice via inhibition of serotonin uptake. Concomitantly, cocaine prevented the maximal producible HTR frequency via simultaneous indirect stimulation of the inhibitory presynaptic 5-HT1A and postsynaptic alpha 2 receptors. In the present study, we have investigated the effects of cocaine and the selective 5-HT (sertraline), norepinephrine (nisoxetine) and dopamine (GBR 12935) uptake inhibitors on the L-tryptophan-induced HTR in the presence of a nonselective monoamine oxidase inhibitor, tranylcypromine. We utilized two experimental protocols where cocaine or sertraline were administered either after (protocol 1) or prior to (protocol 2) L-tryptophan injection. Cocaine potentiated the ability of L-tryptophan to induce HTR to a greater extent in protocol 1, whereas sertraline induced a greater effect in protocol 2. However, in our earlier study cocaine (and also sertraline) up to 10 mg/kg produced a similar degree of potentiation in both experimental protocols on the 5-HTP-induced HTR. Furthermore, as in the latter study on the 5-HTP-induced HTR, in the present investigation nisoxetine potently attenuated whereas GBR 12935 did not modulate the induced HTR. The results show that the respective serotonergic and noradrenergic effects of cocaine also operate on the L-tryptophan-induced HTR. The differential effects of cocaine and sertraline in experimental protocols 1 and 2 on the L-tryptophan- versus 5-HTP-induced HTRs suggest that cocaine has additional effects on the conversion of L-tryptophan to 5-HT.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8831798&dopt=Abstract
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J Neurochem. 1996 Nov;67(5):2204-7.
Combined administration of a 5-hydroxytryptamine (5-HT)1D antagonist and a 5-HT reuptake inhibitor synergistically increases 5-HT release in guinea pig hypothalamus in vivo.
Rollema H, Clarke T, Sprouse JS, Schulz DW.
Central Research Division, Pfizer, Groton, Connecticut 06340-1596, USA.
In vivo microdialysis in guinea pig hypothalamus was used to study the effect of serotonin [5-hydroxytryptamine (5-HT)] subtype 1D autoreceptor blockade on the increase in extracellular 5-HT levels produced by a selective 5-HT reuptake inhibitor (SSRI). Administration of the selective 5-HT1D antagonist GR127935 at 0.3 mg/kg had no effect, but 5 mg/kg significantly increased extracellular levels of 5-HT and 5-hydroxyindoleacetic acid to 135% of basal values. Moreover, at these doses GR127935 significantly attenuated the decrease in extracellular 5-HT levels following local perfusion with the selective 5-HT1D agonist CP-135,807. The SSRI sertraline at 2 mg/kg increased 5-HT levels to 130% of basal levels. The combination of this low dose of sertraline with either dose of GR127935 resulted in a pronounced, long-lasting increases in 5-HT levels to 230% of basal values. These results indicate that the effects of an SSRI on terminal 5-HT are significantly enhanced by coadministration of a 5-HT1D antagonist and confirm that in addition to somatodendritic 5-HT1A autoreceptors, terminal 5-HT1D autoreceptors mitigate the effect of SSRIs on terminal 5-HT. As such, antagonists of the 5-HT1D autoreceptor could be useful as rapidly acting antidepressants and may shorten the onset of antidepressant action when combined with SSRIs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8863532&dopt=Abstract
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