Abstract
Digitonin in association with barium sulphate adsorbable protein solution may play more than one role in the induction of an experimental hypercoagulable state leading to intravascular coagulation. Firstly, it initiates a weak clotting stimulus in vivo; presumably by complexing with cholesterol it brings about the disruption of a lipoprotein complex and the exposure of an active enzyme site. Secondly, this study also demonstrated that digitonin is able to substitute for phospholipid in the acceleration of the clotting stimulus and emphasises the role of micelle-forming substances in the hypercoagulable state.
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Selected References
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