Drugs online research references
Depress Anxiety. 1999;9(2):78-82.
Fluoxetine and sertraline dosages in major depression.
Cantrell R, Gillespie W, Altshuler L.
Department of Psychiatry, UCLA, CA 90095-7057, USA.
In a retrospective study, we sought to determine medication dosages usually prescribed to obtain euthymia in 59 outpatients with a diagnosis of major depression treated with fluoxetine or sertraline. Charts of veterans admitted to the outpatient mental health clinic at the West Los Angeles Veterans Hospital with a diagnosis of major depression and treated with either fluoxetine or sertraline were reviewed. Progress notes were analyzed for a 6-month time period after the initiation of the medication treatment, and improvement was rated by a physician blind to the drug used for treatment. No significant differences were found in overall response rates between the fluoxetine (81% responders) and sertraline (76% responders) groups. Eighty-one percent of the fluoxetine responders compared to 32% of sertraline responders were at the manufacturer's recommended starting dose (MRSD) at the time of clinical response. One-third of patients receiving sertraline were started on or rapidly titrated to more than 50 mg/day. When only those patients receiving an adequate trial of sertraline at 50 mg were considered, 47% required a dose increase to achieve a remission. These data suggest that 50 mg of sertraline may be inadequate for some patients to achieve a resolution of symptoms of major depression and that many clinicians currently prescribe in a manner suggesting that they believe the MRSD is a suboptimal dosage.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10207663&dopt=Abstract
note: kwd match prozac online literature
Endocrine. 1998 Feb;8(1):13-8.
Vasopressin, oxytocin, corticotrophin-releasing factor, and sodium responses during fluoxetine administration in the rat.
Marar IE, Amico JA.
Department of Medicine, University of Pittsburgh School of Medicine, PA 15261, USA.
Hyponatremia has been observed in elderly patients treated with the selective serotonin reuptake inhibitor (SSRI) fluoxetine. The pathogenesis of this effect is not known, but enhanced release of vasopressin (VP) and its renal actions may be a possible mechanism. Excess secretion of VP in combination with large fluid intake is known to induce hyponatremia. We determine if chronic fluoxetine administration in association with liberal fluid intake will induce hyponatremia via enhanced release of VP. We used a previously described model in which fluid intake is forced by administering rats a nutritionally balanced liquid diet. Male Sprague-Dawley rats in groups of 10 were randomized to solid and liquid diets, and each diet group administered daily i.p. injections of fluoxetine (10 mg/kg) or saline for 10 d. Water was given ad libitum to all groups. Daily weight, fluid and food intake, and urine output were measured. On d 10, rats were killed by rapid guillotine decapitation 1-3 h after injection. Trunk blood was collected for measurements of plasma VP and oxytocin (OT) and serum sodium (Na), BUN, creatinine, and glucose. Pituitary glands were assayed for VP and OT content. VP mRNA in the paraventricular and supraoptic nuclei (PVN and SON) and corticotrophin-releasing factor (CRF) mRNA in the PVN were measured by in situ hybridization histochemistry. Fluid intake was significantly higher in groups maintained on liquid vs solid diet (p < 0.0001), as was urine output (p < 0.0001). Fluoxetine-treated rats gained significantly less weight than placebo-treated rats (p = 0.01), in keeping with fluoxetine's anorexigenic properties. However, no significant differences were found among the groups in Na, plasma VP or OT, pituitary VP or OT, or PVN CRF or VP mRNA levels. We conclude that administration of fluoxetine to laboratory rats in the dose and duration used in this study does not significantly affect hypothalamic expression, pituitary stores, or peripheral secretion of VP.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9666340&dopt=Abstract
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Eur J Pharmacol. 1998 May 15;349(1):129-32.
Affinities of venlafaxine and various reuptake inhibitors for the serotonin and norepinephrine transporters.
Beique JC, Lavoie N, de Montigny C, Debonnel G.
Neurobiological Psychiatry Unit, McGill University, Montreal, Canada.
In vitro radioligand binding studies were carried out in rat brain membranes to assess the affinity of various reuptake inhibitors for the serotonin (5-hydroxytryptamine, 5-HT) and the norepinephrine transporters using the selective ligands [3H]cyanoimipramine and [3H]nisoxetine, respectively. The selective 5-HT reuptake inhibitors paroxetine, indalpine and fluvoxamine displayed a high affinity for the 5-HT transporter, whereas the norepinephrine reuptake inhibitor desipramine had a high affinity for the norepinephrine transporter. Duloxetine, a dual 5-HT and norepinephrine reuptake inhibitor, displayed a high affinity for both the 5-HT and the norepinephrine transporters. Interestingly, venlafaxine, a dual 5-HT and norepinephrine reuptake inhibitor, displayed only a moderate affinity for the 5-HT transporter (Ki = 74 nM) and a very low affinity for the norepinephrine transporter (Ki = 1.26 microM). The relatively low affinities of venlafaxine contrast with its potent in vivo 5-HT and norepinephrine reuptake blocking properties. These results raise the possibility that the in vivo effects on the 5-HT and norepinephrine reuptake observed with venlafaxine may not be mediated solely by its binding to the [3H]cyanoimipramine and [3H]nisoxetine binding sites.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9669506&dopt=Abstract
note: kwd match prozac online literature
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