| Indication |
For as an adjunct to coumarin anticoagulants in the prevention of
postoperative thromboembolic complications of cardiac valve replacement
and also used in prevention of angina. |
| Pharmacodynamics |
Dipyridamole, a non-nitrate coronary vasodilator that also
inhibits platelet aggregation, is combined with other anticoagulant
drugs, such as warfarin, to prevent thrombosis in patients with valvular
or vascular disorders. Dipyridamole is also used in myocardial
perfusion imaging, as an antiplatelet agent, and in combination with
aspirin for stroke prophylaxis. |
| Mechanism of action |
Dipyridamole likely inhibits both adenosine deaminase and
phosphodiesterase, preventing the degradation of cAMP, an inhibitor of
platelet function. This elevation in cAMP blocks the release of
arachidonic acid from membrane phospholipids and reduces thromboxane A2
activity. Dipyridamole also directly stimulates the release of
prostacyclin, which induces adenylate cyclase activity, thereby raising
the intraplatelet concentration of cAMP and further inhibiting platelet
aggregation. |
| Absorption |
70% |
| Volume of distribution |
|
| Protein binding |
99% |
| Metabolism |
hepatic |
| Route of elimination |
Dipyridamole is metabolized in the liver to the glucuronic acid conjugate and excreted with the bile. |
| Half life |
40 minutes |
| Clearance |
|
| Toxicity |
Hypotension, if it occurs, is likely to be of short duration, but a vasopressor drug may be used if necessary. The oral LD50 in rats is greater than 6,000 mg/kg while in the dogs, the oral LD50 is approximately 400 mg/kg. LD50=8.4g/kg (orally in rat) |
