TRANSLATIONS FROM CONTINENTAL JOURNALS. 161 
peripheric, must be in direct proportion to the quantity of 
blood the ventricles receive; a deficiency in this would cause 
hyperaemia. The healthy action of the heart, or the attrac¬ 
tion, cannot determine active congestion, if the vascular 
parietes continue to resist the lateral pressure of the blood; 
the moment they give way all is changed and abnormal. 
The third cause which has been evoked, is the peristaltic 
motion of the arteries, grounded on friction. The galvanizing 
of an artery does not cause a vermicular undulation; it is 
only a slow, strong, and persisting contraction, which does 
not extend greatly beyond the part excited. The effect, 
therefore, cannot be propulsion, for the stricture must neces¬ 
sarily repulse the blood to both sides. This stricture, when 
once formed, augments the resistance, the result of which is 
a loss of power. When we intercept the course of the blood 
in an artery, or examine the vessels of a frog^s foot by the 
aid of the microscope, retrograde action is observed. If we 
admit the peristaltic action, it would be necessary to attri¬ 
bute these currents to an antiperistaltic motion, and what 
would then become of the functional regularity of the circu¬ 
lation of the blood ? 
The arguments on which these doctrines are based are 
incompatible with the principles of sound physiology. The 
interpretation of the mechanism of active congestion is inti¬ 
mately bound up with two elements which constitute the 
structure of the arteries. One of these elements is elasticity, 
the other contractility. The former is in the great arterial 
trunks, the latter in the smaller ramifications. The elastic 
fibres in the coats of the arteries, are only physical in action, 
similar to that of caoutchouc, and which persists even after 
death. The arteries dilated by the current of the blood 
contract to their former calibre, and restore to the blood the 
impetus which it had lost in distending them. The division 
of the arterial trunks increases the current of the blood, and 
the friction against the vascular parietes retards the circula¬ 
tion ; thus the undulatory progress of the blood becomes 
more uniform. In the aorta the pulsation is lost. Incrusta¬ 
tion, fatty degeneration, or other structural alteration, will 
destroy the elasticity of the arterial parietes ; they yield no 
longer to the pressure of the column of the blood ; the 
ramifications through the alteration are either inflexible or 
soft, giving way without resuming their original form in either 
case; so that the circulation sustains a local hindrance, the 
arteries admit less blood, and there is anaemia in those organs, 
or if more blood is admitted, the anaemia is changed to 
hyperaemia. 
XXXII. 
22 
