Dipyridamole and other phosphodiesterase inhibitors act as antithrombotic agents by potentiating endogenous prostacyclin

Lancet. 1978 Jun 17;1(8077):1286-9. doi: 10.1016/s0140-6736(78)91269-2.

Abstract

The antithrombotic effect of dipyridamole is through phosphodiesterase inhibition and depends on stimulation of platelet cyclic A.M.P. by circulating prostacyclin in the bloodstream. Low doses of aspirin selectively inhibit platelet cyclooxygenase and potentiate the antithrombotic effects of dipyridamole and theophylline. High doses of aspirin also prevent prostacyclin formation, thereby abolishing the effects of dipyridamole. Thus, the antithrombotic effectiveness of the combination of aspirin and dipyridamole depends critically on the doses used.

MeSH terms

  • Animals
  • Aspirin / administration & dosage
  • Aspirin / pharmacology
  • Blood Platelets / enzymology
  • Cyclooxygenase Inhibitors
  • Depression, Chemical
  • Dipyridamole / administration & dosage
  • Dipyridamole / antagonists & inhibitors
  • Dipyridamole / pharmacology*
  • Dose-Response Relationship, Drug
  • Drug Synergism
  • Epoprostenol / pharmacology
  • Epoprostenol / physiology*
  • Fibrinolytic Agents*
  • Phosphodiesterase Inhibitors*
  • Platelet Aggregation / drug effects*
  • Prostaglandin Antagonists
  • Prostaglandins / physiology*
  • Prostaglandins, Synthetic / pharmacology
  • Rabbits
  • Theophylline / pharmacology
  • Thrombosis / prevention & control*

Substances

  • Cyclooxygenase Inhibitors
  • Fibrinolytic Agents
  • Phosphodiesterase Inhibitors
  • Prostaglandin Antagonists
  • Prostaglandins
  • Prostaglandins, Synthetic
  • Dipyridamole
  • Theophylline
  • Epoprostenol
  • Aspirin