Pharmacologic Effects in Man of a Specific Serotonin-Reuptake Inhibitor

Abstract

Fluoxetine (Li-ly 110140) caused a 63 percent inhibition of [3H]serotonin uptake into platelets obtained from normal volunteers to whom the drug was administered daily for 7 days. This dose had no effect on the usual pressor response produced by injections of norepinephrine or tyramine.

<i>In vitro </i>Histamine and Serotonin Release Studies in Atopic Dermatitis

“…However, the fact that 2 pa tients showed a decreased ability to take up serotonin and that 2 patients showed excep tionally high serotonin-releasing reactions after stimulation with iodipamide might warrant further studies to elucidate the role of platelets in atopic dermatitis. Changes in serotonin uptake have been observed after medication with tricyclic antidepressants [32]; none of our patients had taken these medications, however. Abnormalities of the coagulation system have been described during methacholine-induced inhalation challenge in atopic asthmatics [33], where fi brin split products were detected in arterial and venous plasma.…”

Novel Radiotracers for Imaging the Serotonin Transporter by Positron Emission Tomography: Synthesis, Radiosynthesis, and in Vitro and ex Vivo Evaluation of 11C-Labeled 2-(Phenylthio)araalkylamines

“…[1][2][3][4] In vivo imaging of SERT in living human brain, either by positron emission tomography (PET) or by single photon emission computed tomography (SPECT), has also been pursued vigorously by many groups but has met with limited success. 5 Most of the candidate radiotracers, while possessing high affinity for SERT in vitro, have shown poor ex vivo binding characteristics.…”

Potentiation of the vasospastic response to angioplasty by pretreatment with fluoxetine. A study in the atherosclerotic rabbit.

“…It is important to note that in isolated rat vessels, fluoxetine does not potentiate the vasoconstrictive effects of either norepinephrine or serotonin. In humans, short- 45 or long-term 51 administration of fluoxetine does not appreciably affect a-adrenergic pressor responses. Although it is possible that vasoconstriction was, in part, a result of a lack of Si receptor stimulation in the setting of decreased serotonin release from platelets, exogenous serotonin infusion in these rabbits caused vasoconstriction, suggesting that the S 2 receptor-mediated effects predominate.…”