In vivo platelet aggregation in the rat: dependence on extracellular divalent cation and inhibition by nonsteroidal anti-inflammatory drugs.
Using the Technicon Autocounter, the mechanisms involved in collagen-induced platelet aggregation in vivo have been studied without the interference of an anticoagulant. Extracellular divalent cation was essential for in vivo platelet aggregation. Non-steroidal anti-inflammatory drugs completely inhibited the aggregation induced by collagen in platelet-rich plasma in in vitro or ex vivo studies. In vivo only a maximum of 50% inhibition was achieved when release of thromboxane A2 (TXA2) was completely inhibited. Therefore in vivo, collagen causes aggregation through more than one pathway which operate independently of each other and which are all dependent on extracellular divalent cation. In vivo, when different doses of collagen were compared, aggregation produced by low doses of collagen was more dependent upon prostaglandin endoperoxide/TXA2 formation.
D000758:Anesthesia; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology; D002118:Calcium / Q000097:blood; D002413:Cations, Divalent / Q000502:physiology*; D003094:Collagen / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains; D013929:Thromboxane B2 / Q000097:blood
D000893:Anti-Inflammatory Agents; D001095:Arachidonic Acids; D002413:Cations, Divalent; D016718:Arachidonic Acid; D013929:Thromboxane B2; D003094:Collagen; D002118:Calcium