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      Anisodamine inhibits thromboxane synthesis, granulocyte aggregation, and platelet aggregation. A possible mechanism for its efficacy in bacteremic shock.

      JAMA
      Animals, Cell Aggregation, drug effects, Cricetinae, Depression, Chemical, Granulocytes, Humans, Ibuprofen, pharmacology, Platelet Aggregation, Scopolamine Derivatives, Shock, Septic, drug therapy, Solanaceous Alkaloids, Structure-Activity Relationship, Thromboxane B2, biosynthesis, Thromboxanes, Vasodilator Agents, therapeutic use

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          Abstract

          Anisodamine hydrochloride is a vasoactive drug produced in the People's Republic of China that appears efficacious in clinical and experimental bacteremic shock, and about whose mode of action little is known. Suspecting that the drug might work by inhibition of platelet or granulocyte aggregation, or both, we tested it in these systems. Anisodamine proved a modest inhibitor of granulocyte aggregation and a powerful inhibitor of platelet aggregation; thromboxane synthesis was inhibited in anisodamine-treated platelets, further suggesting that the biochemical mode of action might be inhibition of cyclo-oxygenase or thromboxane synthetase.

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