ON, RHE EAREY STAGES OF INFLAMMATION 243 
in order to explain the remarkable fact, that the blood coagulates within a few 
hours of death in the cavities of the heart and great venous trunks, though it 
retains its fluidity for days in the smaller vessels. Thus in the human subject 
twenty-four hours after death I have found clots in the heart and larger veins, 
including the upper parts of the axillary and femoral trunks, but fluid blood 
in the lower parts of those vessels and all their branches in the limbs. It seemed 
possible at first that this difference might depend on the position of the great 
vessels in the thorax and abdomen, where decomposition begins earlier than in 
the limbs. But this proved not to be the case; for in a horse twelve hours 
after it had been killed, I found the blood fluid in the intercostal and small 
cardiac veins, though coagulated in the vena cava and the coronary vein of 
the heart, which is in that animal of very large size. There being no reason 
to suppose the walls of the larger vessels differently constituted from those of 
the smaller ones, or more lable to undergo post mortem changes, the natural 
interpretation of these facts seems to be that the blood has, even within the 
body, a certain tendency to coagulation, counteracted by an influence exerted 
upon it by the containing tissues, which, operating to less advantage the larger 
the mass of the fluid acted on, fail, at least after death, to prevent it from follow- 
ing its natural course in vessels of a certain magnitude. Again, if we suppose 
that the tissues are merely passive with regard to the blood, it seems difficult 
to understand the rapid solidification of a large quantity shed into a cup. For 
we have seen that mere exposure to the atmosphere will not account for the 
fact ; while at the same time the experiments upon the sheep’s foot indicate 
that an ordinary solid has but a very limited range of operation upon the sur- 
rounding blood,’ and that the clot which it induces does not propagate itself 
to more distant parts; so that the central portions of such a mass of blood 
should remain fluid, unless we admit that, when shed from the vessels, it is 
liberated from an influence which previously kept in check a spontaneous 
proneness to coagulation. Hence it seems likely that a foreign solid intro- 
duced into a vein acts not by creating a disposition to aggregate on the part 
of the fibrine, but by increasing a pre-existing tendency to it (as a thread 
induces the crystallization of sugar-candy), exalting the mutual attraction 
* I find that if a needle is introduced into a vessel and removed after the expiration of about two 
minutes, before any deposit of fibrine has yet occurred upon it, a certain amount of coagulation never- 
theless takes place afterwards in that particular part of the vessel in which the needle had lain. This 
is a curlous circumstance, indicating that an impression leading to coagulation is produced upon the 
blood by contact with an ordinary solid for a shorter time than causes, during its presence, any visible 
solidification. The clot, however, is very slow in forming and very incomplete, so that such cases cannot 
be compared with the perfect and rapid coagulation of a large mass of blood outside the body. Indeed, 
when blood is drawn into a large cup, a great deal of it never touches the side (the ordinary solid) even 
for an instant. 
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