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Rajamani S Eckhardt LL Valdivia CR Klemens CA Gillman BM Anderson CL Holzem KM Delisle BP Anson BD Makielski JC January CT 《British journal of pharmacology》2006,149(5):481-489
BACKGROUND AND PURPOSE: Fluoxetine (Prozac) is a widely prescribed drug in adults and children, and it has an active metabolite, norfluoxetine, with a prolonged elimination time. Although uncommon, Prozac causes QT interval prolongation and arrhythmias; a patient who took an overdose of Prozac exhibited a prolonged QT interval (QTc 625 msec). We looked for possible mechanisms underlying this clinical finding by analysing the effects of fluoxetine and norfluoxetine on ion channels in vitro. EXPERIMENTAL APPROACH: We studied the effects of fluoxetine and norfluoxetine on the electrophysiology and cellular trafficking of hERG K+ and SCN5A Na+ channels heterologously expressed in HEK293 cells. KEY RESULTS: Voltage clamp analyses employing square pulse or ventricular action potential waveform protocols showed that fluoxetine and norfluoxetine caused direct, concentration-dependent, block of hERG current (IhERG). Biochemical studies showed that both compounds also caused concentration-dependent reductions in the trafficking of hERG channel protein into the cell surface membrane. Fluoxetine had no effect on SCN5A channel or HEK293 cell endogenous current. Mutations in the hERG channel drug binding domain reduced fluoxetine block of IhERG but did not alter fluoxetine's effect on hERG channel protein trafficking. CONCLUSIONS AND IMPLICATIONS: Our findings show that both fluoxetine and norfluoxetine at similar concentrations selectively reduce IhERG by two mechanisms, (1) direct channel block, and (2) indirectly by disrupting channel protein trafficking. These two effects are not mediated by a single drug binding site. Our findings add complexity to understanding the mechanisms that cause drug-induced long QT syndrome. 相似文献
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Gillman PK 《Human psychopharmacology》2006,21(2):117-125
A systematic review of published work concerning mirtazapine was undertaken to assess possible evidence of serotonergic effects or serotonin toxicity (ST) in humans, because drug toxicity and interaction data from human over-doses is an useful source of information about the nature and potency of drug effects. There is a paucity of evidence for mirtazapine having effects on any indicator of serotonin elevation, which leads to an emphasis on ST as an important line of evidence. Mirtazapine is compared with its analogue mianserin, and other serotonergic drugs. Although mirtazapine is referred to as a dual-action 'noradrenergic and specific serotonergic drug' (NaSSA) little evidence to support that idea exists, except from initial microdialysis studies in animals showing small effects; those have not subsequently been replicated or substantiated by independent researchers. Also, new data indicate its affinity for Alpha 2 adrenoceptors is not different to mianserin. It appears to exhibit no serotonergic symptoms or toxicity in over-dose by itself, nor is there evidence that it precipitates ST in combination with monoamine oxidase inhibitors, as would be expected if it raises intra-synaptic serotonin levels. Mirtazapine has no demonstrable serotonergic effects in humans and there is insufficient evidence to designate it as a dual-action drug. 相似文献
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A polarized light study of collagen in dermal wound healing 总被引:1,自引:0,他引:1
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A pharmacological overview of opioid mechanisms mediating analgesia and hyperalgesia 总被引:1,自引:0,他引:1
We present a review of the opioid mechanism of analgesia and hyperalgesia and attempt to integrate some of the most recent findings in neuro-anatomy, neuro-physiology and neuropharmacology that indicate the presence of two distinct opioid systems; the one analgesic and the other hyperalgesic. The initial finding of a paradoxical effect of naloxone in which it was able to enhance the analgesic effects of nitrous oxide under certain circumstances led us to postulate the existence of such antagonistic opioid systems which appear to be important in the perception. The review details the further experimental evidence that has subsequently emerged to support our original hypothesis. This includes a hypothesis developed by other workers (viz. diffuse noxious inhibitory control system) which has attempted to explain the analgesic effects of naloxone. Recent anatomical evidence locating the hyperalgesic system in the medullary pontine region is given. 相似文献
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