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Defibrinogenation by batroxobin and acylated batroxobin in rats.

作者信息

Richter M, Paintz M, Stürzebecher J

机构信息

Institute of Pharmacology and Toxicology, Medical Academy, Erfurt, GDR.

出版信息

Folia Haematol Int Mag Klin Morphol Blutforsch. 1988;115(1-2):147-51.

PMID:2459010
Abstract

The thrombin-like snake venom enzyme, batroxobin, was acylated by 4-amidinophenyl benzoate at the active site serine hydroxyl. From the enzymatically inactive benzoyl-batroxobin, batroxobin is generated with a half-life of deacylation of about 1 hour. The clotting activity of benzoyl-batroxobin in plasma is recovered with deacylation. The effect of batroxobin and benzoyl-batroxobin were studied following intravenous injection in rats. Compared to defibrinogenation with batroxobin, that obtained with benzoyl-batroxobin was much retarded. Batroxobin caused microthrombosis initially, which did not develop upon injection of benzoyl-batroxobin in equivalent doses.

摘要

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