The objective was the study of the anticoagulant factors present in vampire bat saliva with the purpose ofestablishing its site of action in the coagulation cascade and its structure. This knowledge is relevant to a better understanding of the phenomena of blood coagulation and the discovery of new anticoagulants with potential clinical use.
The presence of anticoagulant factors in the saliva of blood-feeding bats (vampires) has been suggested by several authors. While a potent plasminogen activator with properties somewhat similar to the tissue plasminogen activator (tPA), have been reasonably characterised biochemically, studies of the presumed anticoagulant factors have been so far inconclusive. The results presented in this summary yield compelling evidence for the existence in vampire saliva of at least one component, different from the plasminogen activator, that is capable of inhibiting blood coagulation. It is clear that this anticoagulant compound is not an antithrombin or a heparin-like substance. The results obtained of the effect of partial purified saliva on the different coagulation assays strongly suggest that a major site of action must be at or below the molecular step dependent on the activity of factor IXa. At present, the precise mechanism of action at this level is not clear. The observation that the anticoagulant effect is also seen on the extrinsic pathway suggested that not only the intrinsic generation of factor Xa was affected, but also the extrinsic and/or the common pathway. This was corroborated by experiments in which the inhibitory effect of poly p-phenylene sulphide (PPS) was directly demonstrated on the amidolytic activity of purified factor Xa on a specific chromogenic substrate. Besides the obvious relevance of this observation, it provides a method of assay for the anticoagulant activity that is, at the same time, highly specific and sensitive.
The immediate effort will now be centred in the purification and structural character isation of the factor involved in the specific inhibition of factor Xa.