Pathological significance of the thromboxane-prostacyclin hypothesis

R. Paoletti, P. Maderna, E. Tremoli

Research output: Contribution to journalArticle

Abstract

Disturbances in the balance between the production of thromboxane A2 by the platelets and that of prostacyclin by the vessel wall may play a major role in disease and be a target for therapeutic agents. Acetylsalicylic acid, given in small doses, may inhibit the production of thromboxane A2, without affecting that of prostacyclin. Even if it reduces prostacyclin synthesis, the drug is beneficial as an antithrombotic agent, possibly because it has actions not related to inhibition of cyclooxygenase. Dazoxiben not only inhibits the production of thromboxane A2 by platelets, but also facilitates that of prostanoids, in part by diverting endoperoxides to the blood vessel wall and to leukocytes. Although reduced production of prostacyclin may contribute to the etiology of atherosclerosis, the blood vessel wall of hypercholes-terolemic animals exhibits an increased production of prostacyclin. The latter has been given successfully in patients with accelerated turnover of platelets or with peripheral vascular disease. However, its very short t1/2 limits its practical use. The availability of stable prostacyclin derivates, such as ZK 36374, may bypass this problem.

Original languageEnglish
Pages (from-to)S179-S185
JournalJournal of Cardiovascular Pharmacology
Volume7
Publication statusPublished - 1985

Keywords

  • Acetylsalicylic acid
  • Arachidonic acid
  • Atherosclerosis
  • Cyclooxygenase
  • Dazoxiben
  • Hypercholesterolemia
  • Lipoxygenase
  • Prostacyclin synthetase
  • Thromboxane synthetase
  • ZK 36374

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

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