[Selective anti-aggregation--a new concept for inhibitors of the platelet function (author's transl)].
Activation and aggregation of platelets, as to their biochemical nature, are two distinct partial mechanisms of platelet reaction. The known inhibitors of platelet aggregation such as acetylsalicylic acid or prostacyclin interfere in metabolic pathways involved in the activation of platelets. In contrast, selective inhibitors of aggregation inhibit the interactions between the surfaces of activated platelets. N-acetylneuraminic acid is an example of a selectively anti-aggregating substance in vitro. Besides its inhibitory effect on the primary aggregation, a platelet-specific inhibition of prostaglandin synthesis belongs to its pattern of effects. By inhibiting the mechanism of aggregation, N-acetylneuraminic acid also inhibits one of the most important trigger of prostaglandin synthesis in platelets. This results in an interruption of the feedback amplification in activation which is mediated by prostaglandin and thromboxane synthesis in human platelets. These properties of anti-aggregating agents combine a favorable pattern of effects with a platelet-specific point of attack.
D001241:Aspirin / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology; D003864:Depression, Chemical; D005340:Fibrinogen / Q000494:pharmacology; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects*; D011453:Prostaglandins / Q000096:biosynthesis; D012794:Sialic Acids / Q000494:pharmacology; D013696:Temperature; D013931:Thromboxanes / Q000096:biosynthesis
D011453:Prostaglandins; D012794:Sialic Acids; D013931:Thromboxanes; D005340:Fibrinogen; D001241:Aspirin; D002118:Calcium
Selektive Aggregationshemmung--Ein neues Konzept für Hemmstoffe der Thrombozytenfunktion.