COAGULATION 



39 



all precautions to prevent alteration of the blood, and immediately 

 separated from the formed elements by the centrifuge, will clot 

 on the addition of tissue extract. The source of the thrombogen 

 has been thought to be the blood-plates, but this has not been 

 proved. Thrombokinase is not present in the circulating plasma. 

 In shed and clotting blood which has not been allowed to come into 

 contact with cut tissues, the only possible sources of thrombokinase, 

 so far as we know, are the corpuscles and the blood-plates. The 

 red corpuscles we may at once dismiss, for although the stromata, 

 especially of nucleated corpuscles, contain thrombokinase, or can 

 under artificial conditions be made to develop that action on 

 coagulation by which we recognize its presence, not only do they 

 remain intact under ordinary circumstances during coagulation, 

 but there is strong evidence, as 

 has already been pointed out, 

 that they do not make any essen- 

 tial contribution to the process. 

 We have left over the leucocytes 

 and the platelets, and it is highly 

 probable that from the platelets 

 thrombokinase is liberated in the 

 first moments after blood is 

 drawn, and, acting on the throm- 

 bogen already present in the plas- 

 ma, changes it into actual throm- 

 bin. This surmise is strengthened 

 by the fact that in freshly shed 

 mammalian blood extensive de- 

 struction of blood-plates takes 

 place. Viewed with the ultra- 

 microscope, the blood-platelets, 

 in a drop of clotting plasma, 



which are at first homogeneous in appearance (optically empty), 

 become granular. Then the platelets begin to agglutinate and 

 swell up, and the agglutinated platelets are transformed into clumps 

 of granules, from which needles of fibrin shoot out. Other needles 

 and filaments of fibrin form in contact with the glass or free in 

 the plasma, and soon the field is occupied by a felt-work of 

 fibrin. The leucocytes have not been observed to be related to the 

 process, at least, in the blood of mammals (Stiibel). It is true that 

 the white layer or ' buffy coat ' which tops the tardily formed clot 

 of horse's blood, and consists of the lighter, and therefore more 

 slowly sinking colourless cells, causes clotting in otherwise in- 

 coagulable liquids like hydrocele fluid much more readily than the 

 red portion of the clot, and yields far more thrombin on treatment 

 with alcohol. It can also be easily verified that in mammalian 



Fig. 6. Fibrin Formationin Plasma from 

 a Case of Haemophilia (Ultramicro- 

 scope) (Stiibel). The needles of fibrin 

 are slowly formed, and very large. 



