Why the study?
Does anisodamine hydrochloride inhibit platelet and granulocyte aggregation and thromboxane synthesis?
Does anisodamine hydrochloride inhibit platelet and granulocyte aggregation and thromboxane synthesis?
Anisodamine inhibits platelet and granulocyte aggregation as well as thromboxane synthesis, providing a possible mechanism for its efficacy in bacteremic shock.
Provides mechanistic insight for anisodamine in bacteremic shock; leaves open translation to human therapy.
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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Ruijuan Xiu (1982) studied this question.
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