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Aspirin pharmacodynamics

Pharmacodynamic alcohol interactions are also of great clinical significance. Additive central nervous system depression with other sedative-hypnotics is most important. Alcohol also potentiates the pharmacologic effects of many nonsedative drugs, including vasodilators and oral hypoglycemic agents. There is some evidence that alcohol also enhances the antiplatelet action of aspirin. [Pg.540]

Yamamoto, K., Abe, M., Katashima, M., Yamada, Y., Sawada, Y., and Iga, T., Pharmacodynamic analysis of antiplatelet effect of aspirin in the literature. Modeling based on inhibition of cyclooxygenase in the platelet and the vessel wall endothelium, Japan Journal of Hospital Pharmacy, Vol. 22, 1996, pp. 133-141. [Pg.418]

O Reilly RA, Sahud MA, Aggeler PM. Impact of aspirin and chlorthalidone on the pharmacodynamics of oral anticoagulant drugs in man. Ann NY Acad Sci 1971 179 173-86. [Pg.997]

In healthy volunteers, steady-state fondaparinux did not alter the pharmacodynamic effects of a single dose of aspirin 975 mg (23). Aspirin did not alter the pharmacokinetics of fondaparinux. [Pg.1438]

FitzGerald GA. Parsing an enigma the pharmacodynamics of aspirin resistance. Lancet 2003 361(9357) 542-4. [Pg.1713]

PHARMACOKINETICS AND PHARMACODYNAMICS Most NSAIDs are rapidly and completely absorbed from the GI tract, with peak concentrations occurring within 1 hours. Aspirin begins to acetylate platelets within minutes of reaching the presystemic circulation. The presence of food tends to delay absorption without affecting peak concentration. Most NSAIDs are extensively protein bound (95-99%) and undergo hepatic metabolism and renal excretion. In general, NSAIDs are not recommended in the setting of advanced hepatic or renal disease due to their adverse pharmacodynamic effects see below). [Pg.439]

Anabolic steroids, aspirin, NSAIDs, quinidine, thyroxine Increased anticoagulant effects via pharmacodynamic mechanisms... [Pg.533]

Cholestyramine interferes with the oral absorption of many drugs (including wrirfarin), resulting in decreased effectiveness. Aspirin and thyroid hormones enhance the action of warfarin via pharmacodynamic mechanisms. Increased anticoagulant effects with cimetidine or quini-dine result from the inhibition of metabolism of warfarin. The answer is (B). [Pg.537]

Modi, N. B. et al.. Pharmacokinetics and pharmacodynamics of TP-9201, a gpllbllla antagonisL administered in combination with Activase t-PA, heparin, and aspirin in beagles, J. Cardiovasc. Pharmacol., 27 105-112, 1996. [Pg.70]

The one pharmacodynamic study below, that also measured gastrointestinal blood loss, found increased bleeding when anti-inflammatory doses of aspirin were given with sodium meclofenamate. ... [Pg.143]

A number of pharmacodynamic studies have investigated whether or not NSAIDs affect the antiplatelet effects of aspirin. Celecoxib 200 mg twice daily, diclofenac 75 mg twice dailyetoricoxib 120 mg daily, lumira-coxib 400 mg daily, meloxicam 15 mg dailynaproxen 500 mg twice daily, parecoxib 40 mg twice dailyand rofecoxib 25 mg daily have all been shown not to alter the antiplatelet effects of aspirin in doses of 75 to 325 mg daily. The effects of ibuprofen ate less elear, and may be related to the order of drug administration. [Pg.144]


See other pages where Aspirin pharmacodynamics is mentioned: [Pg.35]    [Pg.113]    [Pg.765]    [Pg.655]    [Pg.772]    [Pg.139]    [Pg.738]    [Pg.152]    [Pg.332]    [Pg.1013]    [Pg.1712]    [Pg.2573]    [Pg.915]    [Pg.246]    [Pg.68]    [Pg.381]    [Pg.283]    [Pg.381]    [Pg.177]    [Pg.668]    [Pg.155]    [Pg.303]    [Pg.813]    [Pg.451]    [Pg.1119]    [Pg.37]    [Pg.279]    [Pg.1235]    [Pg.108]    [Pg.381]    [Pg.133]   
See also in sourсe #XX -- [ Pg.32 , Pg.45 ]




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