78 ON SPONTANEOUS GANGRENE FROM ARTERITIS AND 
the same chemical tendencies as we have seen it to possess when removed from 
the body; and those parts of the fluid which remained at rest under these 
conditions, namely, the motionless layer of liquor sanguinis next to the lining 
membrane, and the portions of blood in the sinuses of the valve, underwent 
coagulation, yielding up their ammonia through the permeable coats of the vein. 
And I think we need not hesitate to admit that similar occurrences take place 
in the early stages of arteritis and phlebitis, the coats of the vessels being in 
those cases not dead, but impaired in vital energy by inflammation. 
A similar explanation appears to account for the early formation of coagula 
in the vicinity of a ligature placed upon an artery. It has been seen how utterly 
the usual explanation, that of the quiescence of the blood, fails to account for 
the phenomenon; but the fact that lymph is afterwards exuded from this 
part of the vessel shows that the case is really one of limited traumatic arteritis. 
But if the coagulation within inflamed vessels thus receives a solution 
from the results of the last-mentioned experiment, still more unequivocally, 
at least to most of my hearers, is the coagulation in gangrene explained, such 
as occurred, for instance, in the case which has been described. 
Again, it is well known that contused wounds bleed very little, the ends of 
the divided arteries becoming speedily plugged with a long coagulum. The 
only explanation which Sir Charles Bell could offer of this remarkable provision 
of nature was, that the living vessels had a special faculty of preventing the 
blood from exercising friction upon their lining membrane, but that the con- 
tused artery, having lost its vitality, the blood became arrested by friction 
and coagulated. We now see that there was much more truth in this theory than 
has been generally supposed, though the loss of vitality in the vessel does not 
operate in the manner which Sir Charles imagined. 
It has been found difficult to understand why the fact of the arteries being 
converted into calcareous tubes should impress upon the blood within them 
a tendency to coagulate in atheromatous degeneration of the vessels. The 
impairment, or entire loss of vitality connected with such a condition, will now 
be found a sufficient explanation. 
The coagulation in aneurysm is now equally comprehensible, the walls of 
the sac consisting either of degenerated or torn coats of the vessel, of inflamed 
surrounding tissues, or of layers of fibrine, each of these constituents being in 
a state of very low vitality. 
The rapid coagulation of lymph, which appears to be neither more nor less 
* I find I have not done justice to Sir C. Bell’s views upon this subject. In his later works he ex- 
presses the opinion that the lining membrane of the living vessels possesses the power of ‘ preserving 
the blood fluid ’, and that the cause of coagulation in a contused artery is the loss of this power in con- 
sequence of the injury.—Vide Sir C. Bell’s Institutes of Surgery, vol. i, p. 52, and vol. il, p. 277. 
