THE BLOOD 263 



termed anti-thrombin. So long as this relation is not disturbed the blood 

 remains fluid. When blood is shed there is supposed to develop from the cell 

 elements of the blood, the leukocytes and blood-platelets, and perhaps from 

 the cell elements of the injured tissues as well, a plastin, the specific action of 

 which is to combine with the anti-thrombin and thus set free the prothrombin. 

 This having been accomplished the calcium salt activates the prothrombin, 

 and converts it into thrombin, after which it combines with the fibrinogen. 

 For this reason the plastic agent has been termed thrombo-plastin. Experi- 

 ments indicate that this agent belongs to the group of bodies known as 

 phosphatids and similar in its properties to one member of this group, viz., 

 kephalin. So long as the relations of the blood and the vascular apparatus 

 remain physiologic, no coagulation occurs in the vessels. The reasons 

 assigned for this are: (i) the absence of thro mboplas tin (kephalin); 

 (2) the presence of anti-thrombin. Recently Howell has enlarged and 

 supplemented the foregoing explanation for the fluidity of the blood by 

 introducing two new substances in the blood, viz.: pro-anti- thrombin 

 and heparin. The pro-antithrombin, the antecedent of anti-thrombin, 

 is present in the plasma and serum in considerable quantity and is capable 

 of being converted into antithrombin, under certain conditions, one 

 condition being the entrance into the blood of a phosphatid obtained 

 from the liver and termed, therefore, heparin. Heparin on entering the 

 blood is supposed to activate the pro-antithrombin to active antithrombin 

 as well as to inhibit the conversion of prothrombin to thrombin and thus 

 maintain the fluidity of the blood and prevent intravascular coagulation. 

 When blood is shed, then the thrombo-plastin, kephalin, is developed where- 

 upon the heparin activity is overcome and coagulation at once occurs. 



Intra-vascular Coagulation. Whenever the blood-vessel and espe- 

 cially the lining membrane is injured as by ligation or tearing or in any 

 other way, coagulation promptly takes place, with the subsequent occlu- 

 sion of the vessel, and in consequence of the development of kephalin. 



Under pathologic conditions of the circulatory apparatus, especially of 

 the internal lining, intra-vascular coagulation frequently arises, though the 

 process cannot be considered as identical with extra- vascular coagulation. 

 Many pathologists assert that in its origin, mode of formation, and structure 

 the intra-vascular coagulum or thrombus is not a true coagulum as ordinarily 

 understood, but rather a conglutination of blood-plaques and leukocytes. 

 Whenever the integrity of the internal wall of the vessel is impaired by 

 disease or by the introduction of foreign bodies, there is primarily a deposition 

 and accumulation of blood-plaques at the injured area or on the foreign body 

 which constitutes to a large extent the mass of the thrombus which at once 

 forms. The thrombi which form on the surface of atheromatous ulcers, on 

 the valves of the heart, and in the veins in consequence of diseased states, on 

 threads or needles passed through the vessels, at the orifices of torn blood- 

 vessels, consist largely of blood-plaques. A thrombus so formed may con- 

 tain a number of delicate fibrin threads, which, however, present a different 

 appearance from the fibrin of the extra-vascular clot. In the thrombi which 

 form around foreign bodies there is a larger quantity of fibrin than in those 

 originating from causes wholly within the vessel. 



