Abstract
Conclusion
It has long been established that thrombin, once formed, is active in the presence of excess of oxalate, etc., this being the classical experiment in support of the view that ionized calcium is not necessary for the clotting process proper (“second phase” of Hammarsten). It is less widely appreciated that clotting under these conditions is definitely slower than normal. Forty years ago Hammarsten 3 failed to inactivate thrombin by oxalation, and Kastl 4 and Eagle 5 have recently confirmed. The divergent findings of Loucks and Scott 2 are supported by the present experiments. Since the data appear to be unequivocal, and since their importance in the elucidation of the calcium factor in coagulation is obvious, it is imperative that further investigations be made with a view to explaining the discrepancies in the literature and elucidating further the mechanism of action of the so-called “decalcifying” anticoagulants.
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