THE CLOTTING OF THE BLOOD OF AN AMPHIBIAN, <i>BUFO MARINUS</i> LINN

Abstract

SUMMARY Investigation of the intrinsic thromboplastic activity of the blood of the toad Bufo marinus Linn. shows that this arises largely from the blood leucocytes. More prothrombin appears to be consumed in leucocyte‐rich than in leucocyte‐free mixtures. A spreading change which occurs in the toad thrombocyte (a spindle‐shaped leucocyte) on contact with certain surfaces is morphologically analogous to the “viscous metamorphosis” which occurs in the human platelet. However, the change in the thrombocyte is not inhibited by decalcifying anticoagulants or heparin and takes place on plain glass, siliconed glass and perspex; somewhat less rapidly on cellulose acetate; and not at all on paraffin wax or polyethylene. The thromoplastic activity of plasma‐free leucocytes appears after contact with glass, siliconed glass, or perspex, but not after contact with paraffin wax, and so the development of the leucocyte thromboplastic activity after surface contact runs parallel to the morphological change observed in the thrombocytes. A non‐cellular plasma co‐thromboplastic factor activated by contact with glass (but not siliconed glass) is also found. It does not depend on calcium ions for its activation or for its activity. It reacts with the thromboplastin released by glass‐treated or siliconed‐glass‐treated leucocytes to convert it to a still more active thromboplastin, this conversion itself being accelerated by the presence of a glass (but not by a siliconed glass) surface. An alumina‐adsorbable serum accelerator appears after clotting and a serum anticoagulant is also found. The plasma co‐thromboplastic contact factor has properties comparable to those of human Hageman factor, and the serum accelerator to those of human Christmas factor. The findings are discusseed in relation to a possible stage in the evolution of the human blood coagulation system. A scheme for the coagulation mechanism of the blood of Bufo marinus is presented (Fig. 1).