On the mechanism of salicylate-induced hypothrombinaemia.
The mechanism of salicylate-induced hypothrombinaemia has been investigated in the rabbit. Administration of methyl salicylate produced a significant decrease in prothrombin complex activity, in the activity of clotting factors II, VII and X but no significant change in factor V activity. Metabolic studies with [3H]vitamin K1 showed that salicylate increased the plasma concentration ratio of [3H]vitamin K1-epoxide: [3H]vitamin K1. The results are consistent with the concept that salicylate produces its anticoagulant effect, like the coumarin anticoagulants, by interruption of the physiologically important vitamin K1-epoxide cycle at the epoxide reductase.
D000818:Animals; D004852:Epoxy Compounds / Q000378:metabolism; D008297:Male; D011516:Prothrombin / Q000032:analysis; D011817:Rabbits; D012459:Salicylates / Q000097:blood / Q000494:pharmacology*; D013917:Thrombin / Q000172:deficiency*; D010837:Vitamin K 1 / Q000378:metabolism
D004852:Epoxy Compounds; D012459:Salicylates; D010837:Vitamin K 1; D011516:Prothrombin; D013917:Thrombin