v THE BLOOD: PLASMA 133 



retards coagulation ; as shown by the fact that when the shed 

 blood is warmed to the ordinary temperature of the animal 

 (37-3S C.) it x;lots more rapidly (Hewson). 



Coagulation does not depend on the quiescence of the blood 

 drawn from the vein, for some of the blood in the dog's heart 

 13 hours after death (Hewson), and the whole of a dog's blood 

 6|-7| hours after death by asphyxia, is found to be fluid. 

 Again, the blood in a tortoise heart that has been ligatured or 

 excised, and kept at a temperature of approximately zero, is found 

 to be fluid 7-8 days after (Briicke). 



Nor, again, does coagulation depend on contact with the air or 

 its oxygen, for the blood received under a bell-jar filled with 

 mercury coagulates, and the blood of a tortoise does not clot after 

 injection of a considerable quantity of air into its vessels (Briicke). 



Contact with the normal, living walls of the vessels inhibits 

 coagulation of the circulating blood, while the injury or death of 

 the vascular endotheliurn, or the introduction of any foreign body 

 into the vessels (e.g. a needle pushed through the heart of a living 

 tortoise), make the blood coagulate (Briicke). 



When the blood is received directly into a vessel greased 

 with vaseliu, or under oil, it neither adheres to it nor clots, nor 

 does it on stirring with a well-greased glass rod. On the other 

 hand, it coagulates readily when stirred with a rod that has 

 not been greased, or when any foreign body is introduced which 

 the blood can adhere to. It is therefore highly probable that the 

 circulating blood remains fluid because its morphological elements 

 do not adhere to the normal endotheliurn of the vessels, and that 

 a thrombus is formed whenever such adhesion becomes possible 

 by degeneration of the endotheliuni (Durante) or other morbid 

 lesions of the internal walls of the vessels and heart, as, e.g., 

 in phlebitis, endocarditis, eudarteritis, atheromatosis (Freund, 

 1886). 



(6) The second question to lie solved is the determination of 

 the immediate cause of coagulation, i.e. why the simple adhesion 

 of certain elements of the blood to foreign bodies, or to the injured 

 endotheliurn, should give rise to the formation of fibrin. 



In this connection we have a series of striking observations, 

 which show plainly that the formation of the fibrin clot is intimately 

 bound up with the functional alteration or destruction of the 

 formed elements of the blood, more particularly of the leucocytes, 

 which, as we have seen, are very unstable, and easily damaged by 

 every imaginable external physical influence. Simple contact with 

 foreign bodies, to which they may adhere, is sufficient to provoke 

 secretion in the plasma of substances able to produce clotting. 



This theory, proposed by Addison (1841) and Beale (1864), was 

 clearly demonstrated for the first time by Mantegazza (1876). 

 Wherever a thrombus is produced within the vessels or the heart, 



