PATHOLOGICAL ANATOMY. 
375 
ternal coat, especially at the periphical end, and around the point 
of the clot. Abrasions of the elastic internal coating and granu- 
lations of the middle coat exist, but this cellular proliferation re¬ 
mains insignificant, and seems to be principally designed to unite 
the clot more intimately to the internal face of the vessel. Inter¬ 
nally, the embryonary tissue has accumulated sufficiently to en¬ 
velop the ligation with a fusiform mass. If the wound heals by 
the first intention, it forms a thick true muff, or external callus. 
The cells that compose it penetrate between the fibres of the 
adventitious tissue, and disintegrate and resorb the fasciculus 
of fibres which are surrounded by the ligature. Both ends of 
the blood vessel separate, ending by a well closed cul-de-sac, and 
the encysted thread is resorbed or eliminated. 
(Second Period. During the third week the embryonary tissue 
has so far penetrated the internal and middle coats that they sep¬ 
arate slightly, the extremities of the vessels opening and allow¬ 
ing this embryonary tissue to enter the interior of the vessel. 
The critical moment is that when secondary hemorrhage occurs, 
which may be anticipated in case of the suppuration of the ex¬ 
ternal callus. The new tissue penetrates the inferior layers of 
the callus, and disintegrates it in forming an internal callus, 
which is rich in capillaries derived from the external callus. 
Third Period. The temporary tissue is now resorbed, and 
is succeeded by a definitive cicatricial structure. While the inflam¬ 
matory tissue is resorbed on the outside of the vessel, a cellular 
differentiation takes place on the inside. Fusiform cells, with 
nuclei in rods, appear and remain, to form in the cicatrization, a 
new muscular layer. These, in the places where the internal 
elastic coat is abraded, mingle with those of the middle coat, 
meeting each other at right angles. 
The cicatrix is always so arranged as to produce a gradual 
- stricture of the artery, and to change it into arterial substance. 
In very large arteries the cicatrix elongates and is transformed 
into cavernous tissue. 
The researches of the author tend to show that, contrary to 
the old theory which attributes the obliteration to the thickening 
of the internal coat, it is the middle coat which contributes the 
