May increase plasma concentration and CV effects of adenosine. Enhances effects of oral anticoagulants and produces additive effects w/ other anti-platelets (e.g. aspirin). May increase hypotensive effect of BP lowering drugs. May counteract anticholinesterase effect and aggravate myasthenia gravis when used w/ cholinesterase inhibitors. May reduce the efficacy of fludarabine. Reduced absorption w/ antacids. Abolished coronary vasodilation w/ xanthine derivatives (e.g. theophylline, aminophylline, caffeine) during myocardial imaging.
Description: Dipyridamole, a platelet aggregation inhibitor, causes an accumulation of adenosine, adenine nucleotides, and cyclic AMP by inhibiting the activity of adenosine deaminase and phosphodiesterase, thus inhibiting platelet aggregation and producing vasodilation. Addtionally, it stimulates the release of prostacyclin or PGD2 and causes coronary vasodilation. Pharmacokinetics: Absorption: Incompletely absorbed from the GI tract. Time to peak plasma concentrations: Approx 75 min. Distribution: Widely distributed into body tissues. Crosses the placenta in small amounts and enters breast milk. Volume of distribution: 2-3 L/kg. Plasma protein binding: 91-99%, mainly to α1-acid glycoprotein. Metabolism: Metabolised in the liver to glucuronide conjugate; may undergo enterohepatic recirculation. Excretion: Via faeces (as glucuronide conjugates and unchanged drug). Terminal elimination half-life: 10-12 hr.
Store between 15-25°C. Do not freeze. Protect from light.
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