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1. |
Fluoxetine: A Serotonin‐specific, Second‐generation Antidepressant |
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Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy,
Volume 7,
Issue 1,
1987,
Page 1-14
Roger W. Sommi,
M. Lynn Crismon,
Charles L. Bowden,
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摘要:
Fluoxetine is a bicyclic antidepressant that is a specific and potent inhibitor of the presynaptic reuptake of serotonin. It has essentially no effect on the reuptake of norepinephrine or other neurotransmitters. Similarly, it has negligible binding affinity for neurotransmitter receptor sites. It is well absorbed after oral administration, with absolute bioavailability in dogs of approximately 72 ± 27.6%. The mean Tmaxis between 4 and 8 hours, and it is approximately 94% protein bound. After a single dose, the elimination half‐life is 1–3 days. After long‐term administration, the elimination half‐life averages 4 days. Its pharmacokinetics appear nonlinear. It is metabolized to an active metabolite norfluoxetine, which is also specific for the inhibition of serotonin reuptake. Norfluoxetine's elimination half‐life averaged 7 days after long‐term administration. Little is known about potential drug interactions; however, fluoxetine appears to have minimal clinically relevant interactions. Fluoxetine is indicated in the treatment of major depression. Its efficacy is comparable to the tricyclics and it has a similar onset of action. Although doses as high as 80 mg/day have been used, the optimal dosage range appears to be 20–40 mg once daily. Fluoxetine has been used with success in obsessive‐compulsive disorder and intention myoclonus, however, its use in these disorders remains investigational. The frequency of side effects is low and dose related; the most common effects are nausea, anxiety, insomnia, anorexia, diarrhea, nervousness, and headache. Eight reports of intentional overdose with fluoxetine alone resulted in no deaths and mild adverse effects. It will be marketed as 20‐mg capsules under the brand name of Prozac. Although fluoxetine should be added to formularies, its use should be reserved for treatment of those who do not respond to or do not tolerat
ISSN:0277-0008
DOI:10.1002/j.1875-9114.1987.tb03496.x
出版商:Blackwell Publishing Ltd
年代:1987
数据来源: WILEY
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2. |
Commentaries: Commentary 2 |
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Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy,
Volume 7,
Issue 1,
1987,
Page 14-15
Alan J. Gelenberg,
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ISSN:0277-0008
DOI:10.1002/j.1875-9114.1987.tb03498.x
出版商:Blackwell Publishing Ltd
年代:1987
数据来源: WILEY
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3. |
Commentaries: Commentary 3 |
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Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy,
Volume 7,
Issue 1,
1987,
Page 15-15
John M. Patrias,
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ISSN:0277-0008
DOI:10.1002/j.1875-9114.1987.tb03499.x
出版商:Blackwell Publishing Ltd
年代:1987
数据来源: WILEY
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4. |
Carprofen: A New Nonsteroidal Antiinflammatory Drug Pharmacology, Clinical Efficacy and Adverse Effects |
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Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy,
Volume 7,
Issue 1,
1987,
Page 16-24
William M. O'Brien,
George F. Bagby,
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摘要:
Carprofen (Rimadyl, Roche), a new nonsteroidal antiinflammatory drug (NSAID) will soon be commercially available. Not counting aspirin and other salicylates, there arenow at least a dozen NSAIDs commercially available in the United States.
ISSN:0277-0008
DOI:10.1002/j.1875-9114.1987.tb03500.x
出版商:Blackwell Publishing Ltd
年代:1987
数据来源: WILEY
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5. |
Commentary |
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Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy,
Volume 7,
Issue 1,
1987,
Page 24-24
William A. Parker,
Ingrid S. Sketris,
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ISSN:0277-0008
DOI:10.1002/j.1875-9114.1987.tb03501.x
出版商:Blackwell Publishing Ltd
年代:1987
数据来源: WILEY
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6. |
Risks and Indications of Phenylbutazone: Another Look |
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Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy,
Volume 7,
Issue 1,
1987,
Page 25-27
Gerald A. Faich,
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摘要:
In 1984 an extensive review of phenylbutazone risks was undertaken by the Food and Drug Administration (FDA). Since that review, new recommendations for the drug's use have been published. Marketed in 1952, phenylbutazone has long been recognized as capable of inducing aplastic anemia. The risk of marrow depression is greatest in elderly females treated for over a month. Overall, the risk does not exceed that of many commonly used drugs (e.g., penicillin, which induces anaphylaxis). Nonetheless, phenylbutazone should not be a drug of first choice and should not be used for minor, self‐limited condition
ISSN:0277-0008
DOI:10.1002/j.1875-9114.1987.tb03502.x
出版商:Blackwell Publishing Ltd
年代:1987
数据来源: WILEY
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7. |
Molsidomine: Alternative Approaches To Treat Myocardial Ischemia |
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Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy,
Volume 7,
Issue 1,
1987,
Page 28-37
Rolf‐Eberhard Nitz,
Volker B. Fiedler,
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摘要:
The long‐acting antianginal drug molsidomine has been shown experimentally to reduce myocardial infarct size when administered prior to or after cardiac insult. This is due to several drug actions.1. Dilation of postcapillary capacitance vessels diminishes venous return, preload, heart dimensions, and myocardial oxygen consumption. 2. Relaxation of stenosed conductive coronary arteries increases the perfusion of myocardial areas at risk of infarction due to enhanced collateral circulation. 3. Increased regional blood supply nourishes predominantly subendocardial cardiac muscles as a result of reduction of extravascular coronary pressure, and resistance. 4. The stable heart rate and cardiac contractility favor improved heart performance. 5. The inhibition of platelet aggregation in vivo by molsidomine or its active metabolites, SIN‐1 and SIN‐1A, is linked to the stimulation of prostacyclin synthesis, inhibition of thromboxane release with induction of thrombosis and vasoconstriction, and enhanced concentrations of cyclic guanosine monophosphate. 6. Dilation of coronary arteries after intracoronary administration of SIN‐1, with inhibition of platelet aggregation by restrained release of adenosine diphosphate and stabilization of platelet membranes, facilitates the recanalization of stenosed arteries and reduces coronary muscle tone at the site of thrombosis. 7. Activation of the human fibrinolytic system and drug‐induced release of a plasminogen activator favor dysaggregatory effects. 8. The drug's inhibiting actions on lipoxygenase products of arachidonate (e.g., 12‐hydroperoxy‐eicosatetraenoic acid and leukotrienes) may shift prostaglandin catabolism to cyclooxygenase products (e.g., prostacyclin) that protect against the expansion of ischemia and the induction of coronary spasm.Experimentally, the hemodynamic effectiveness of molsidomine can be antagonized by catecholamines (afterload effects) and dihydroergotamine (preload and afterload effects) respectively. Further clinical investigations will clarify the application of these mechanisms for the therapeutic success of the drug in human myocardi
ISSN:0277-0008
DOI:10.1002/j.1875-9114.1987.tb03503.x
出版商:Blackwell Publishing Ltd
年代:1987
数据来源: WILEY
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