326 
ON INFLAMMATION. 
part is one of the most valuable and the surest guides to the 
actual seat, and the intensity of the malady. It can be well 
understood, if the definition of inflammation already given be 
admitted, why increased heat should be a necessary consequence 
of inflammation. In the capillaries the blood is changed from 
arterial to venous; and, being so changed, among other im¬ 
portant consequences, it lost s a portion of its capacity for 
heat: it cannot combine with so much heat and hold it in a latent 
state,—a portion of the caloric which it before contained there¬ 
fore escapes, and as the capillaries are found in every part of the 
frame, there is every where a laboratory for the production of 
animal heat. Under inflammation, more blood is sent through 
the capillaries of the part,—more blood is changed from arte¬ 
rial to venous—more heat is therefore extricated, and that in pro¬ 
portion to the extent and the degree of the inflammation, or, in 
other w ords, the additional quantity of blood that is carbonized. 
Now, if inflammation be “ an increased action of the heart and 
arteries, while the capillaries are in their natural state,” accord¬ 
ing to Dr. Hastings, there can be no additional formation of 
venous blood, and no additional extrication of heat. 
If, according to Boerbaave, the blood is obstructed from its 
thickness and viscidity; or, according to Cullen, the vessels are 
contracted or spasmed; or, according to Allen, they are debilitated 
and relaxed ; or, according to Dr. Philip, there is a diminished 
action of the capillaries, then there cannot be the usual change 
from arterial to venous blood: there is not the usual quantity of 
blood exposed to the process, and coldness instead of heat ought 
to be the character of inflammation. When the vital current lags, 
the temperature of the part is diminished; and when it is arrested 
in its course, the coldness of death ensues. 
The actual temperature of the fram^, however, is not mate¬ 
rially raised. It is only that of the skin. The animal body is sur¬ 
rounded by a medium—atmospheric air—usually of a tempera¬ 
ture much low er than itself, and, from the tendency of free calo¬ 
ric to an equilibrium, rapidly stealing from it a great portion of 
the heat evolved in the change of the blood. The skin, there¬ 
fore, or that portion of it exposed to the atmosphere, is of a 
considerably lower temperature than that of the frame. But 
when the heat is evolved with greater rapidity, from the change 
of a larger quantity of blood from an arterial to a venous state, 
the surrounding air cannot immediately combine with the whole 
of it, nor can the temperature of the skin be so much lowered. 
If the inflammation be ever so intense, the circumambient air will 
take away a portion of heat from the skin, and the temperature 
of the integument immediately over the seat of inflammation 
