It has already been shown that in the normal condition there exists only a very small amount of fibrous tissue between the fenestrated membrane of Henle and the endothelial lining of a mediumsized artery; it is difficult even to see it except in a thin, well-prepared section. It has also been shown that the effect of chronic inflammation on fibrous tissue is to cause it to increase and grow.

In chronic endarteritis some morbid substance circulating in the blood sets up a chronic inflammatory process in the small amount of fibrous tissue normally existing between the membrane of Henle and the endothelial lining, and causes it to increase gradually. This can easily be made out if an artery is taken where the fibrous tissue is increasing, and before it becomes dense by contraction. The result is a growth of fibrous tissue in many cases as thick or thicker than the muscular coat of the artery. This change takes place without affecting the tunica media, as the comparison of a large number of arteries taken from healthy subjects with the same arteries in cases of chronic endarteritis has shown that there is no hypertrophy of the muscle coat, the increased growth being confined to the intima. The change also is a general one, and is as well seen in the basilar artery as in an intrinsic artery of the kidney.

ATHEROMA.

This condition is found more especially in the larger arteries and the aorta. It is a combination of the various disease processes already described. There may have been an attack of acute inflammation affecting small portions of the lining membrane; this may pass into the chronic form, producing raised plaques of hard fibrous tissue. Or there may be the degeneration already described, in which new fibrous tissue is formed, followed by softening or calcification, with the result of either forming an atheromatous abscess or a so-called bony plate. The histological characters vary with the condition in the manner already shown.

SENILE GANGRENE: CONDITION OF THE VESSELS.

The changes in the vessels vary in different parts, and the following description is based on the dissection and microscopic examination of a number of cases.

The femoral artery is generally in an advanced stage of calcification, and the lime salts must be removed before sections can be cut.

After decalcification the artery shows marked degeneration. The muscular coat is broken up in places where the calcification existed, so that the muscle fibres cannot be made out; in some parts the process has not gone so far as in others; but in all, where calcification has taken place the normal structure is lost. The adventitia remains unaffected.

In the intima there is an irregular growth of fibrous tissue between Henle's membrane and the endothelial lining, causing a decrease in the calibre of the vessel.

The femoral vein shows changes of a different character. Under the endothelial lining a new formation of fibrous tissue has taken place, which extends into the lumen of the vessel in an irregular manner. This tissue consists of a homogeneous matrix containing branched cells in those parts nearest the lumen, while the other parts next the middle coat of the vein contain a quantity of white fibrous tissue. This growth is most unevenly distributed round the lumen of the vessel, in some parts there being none, in others the growth is thicker than the original wall of the vessel. It is interesting to note that while the morbid process reduces the lumen of the artery, the lumen of the vein is also reduced.

In the popliteal artery and vein the same changes are seen. The new formation in the intima is here very large, and the process of fatty degeneration well shown. In parts there is dense fibrous tissue formed containing a large supply of capillary vessels of irregular formation; in other parts every stage of degeneration can be seen, the fatty process being represented by large yellow masses formed from the degeneration of the connective tissue corpuscles. The fibrous tissue itself seems to undergo a process of liquefaction, and the product becomes fixed in the process of hardening; this produces a number of cracks which look exactly like acicular crystals. There is no appearance of cholesterin anywhere.

In the anterior and posterior tibial arteries and their venæ comites, as well as in all the small branches from them, the most varied changes have taken place.

In some cases the vessels are blocked up with blood-clot, and this is sometimes quite recent; in others, of old standing, with several small vessels running through it. In the fresh clot the process of organization can be well studied. In the centre the mass looks yellow and the blood corpuscles can be easily made out. Toward the periphery fibrin is formed and capillary bloodvessels are penetrating it; these vessels can be distinctly traced to others in the muscular

coat. In these vessels filled with fresh clot the membrane of Henle is not thrown into folds by the contraction of the muscle coat, that is, the presence of the clot prevented post-mortem contraction of the muscular coat. In the old clot the organizing process has resulted in filling the lumen of the vessel with fibrous tissue, in which is a quantity of brown pigment, and through which run a number of small vessels. These vessels are evidently sufficient to keep up some circulation through the original vessel, and the membrane of Henle, which is much thickened is thrown into folds; the muscular coat, although it had undergone degeneration in part, is yet in a healthy condition in other parts. This shows that, although the vessel had been closed up by blood-clot, yet vessels had formed in it by which the circulation could still be maintained, although immensely reduced in quantity. It also shows that the muscular wall could still retain some functional activity even after the lumen of the vessel was filled with organized clot.

Other branches showed the changes already described; they all consist in degeneration and calcification of the muscle coat and growth of fibrous tissue in the intima.

In the veins the change is very marked, but always consists of a new formation of fibrous tissue, akin to gelatinous or embryonic, and as this grew older more fibrous tissue formed in it and it became denser.

The valves were also involved in the change, and in many cases had become thickened throughout, and often irregularly, showing masses of dense fibrous tissue in their substance.

All vessels, both arteries and veins, large and small, show some change by which their calibre had been greatly reduced. And this change could, in several of the cases, be made out to be of different

ages.

As has already been shown, old clot and recent clot existed side by side; so in the veins, fibrous tissue could be seen which had formed and then contracted into a dense band, and on this was a formation of young fibrous tissue-showing that whatever had been the cause of this growth, it had existed at some former time, had been removed, and then again set up.

VARICOSE VEINS.

In varicose veins the vessel wall becomes much thickened; on making a section of one of these vessels this thickening is found to

be unilateral, so that one side of the wall may be four or five times as thick as the other.

This thickening is produced by the formation of new fibrous tissue. This growth commences in the same manner as already described, by the formation of tissue, like embryonic, which as it gets older becomes much denser from the increased amount of fibrous tissue formed in it.

In varicocele the same change is found, but is, if anything, more uniform, and it sometimes extends around the whole wall of the vessel.

In both these conditions the valves are much altered and thickened, the valves of a small vein becoming nearly as thick as the normal wall; they also are enlarged unevenly, in some places being twice as thick as in others. A small portion of a vein may be enlarged from an acute inflammation in its lining membrane becoming chronic and setting up fibrous growth at this spot. The tissue formed resembles that already described.

CHAPTER XXVII.

DISEASES OF THE RESPIRATORY ORGANS.

INFLAMMATORY CONDITION OF THE RESPIRATORY PASSAGES.

In the normal condition the mucous membrane of the respiratory passages consists of

A layer of ciliated columnar epithelium; this is formed of cells two or three deep, the upper row of which is ciliated, fixed on a thick basement membrane.

Under this is the mucous membrane formed of loose connective tissue, with a number of lymph corpuscles and diffuse adenoid tissue.

Next comes a layer of yellow elastic tissue arranged longitudinally. Then the submucous tissue, in which lie numerous mucous and serous glands; then the cartilage.

This may be taken as a general description of the mucous membrane of the larynx and trachea; there are slight modifications in the arrangement of the elastic tissue and situation of the mucous glands in different parts. It must also be remembered that both surfaces of the epiglottis and the true vocal cords are covered with stratified squamous epithelium, and also the inner surface of the arytenoid cartilages.

The normal structure of the bronchi is very similar to that in the trachea, but differs in having a circular band of non-striped muscle lying between the mucous and submucous coats. The arrangement of the cartilage is also different, as the semilunar rings of the trachea are broken up into pieces of cartilage which surround the whole tube.

In examining a lung in the collapsed condition, sections passing through a bronchus show the mucous membrane thrown into folds by the contraction of the muscle coat.

When the respiratory passages in a case of inflammatory disease, such as bronchitis, are examined, the changes produced by inflammation can be easily made out.

It will at once be seen that the mucous membrane is much swollen and that the vessels are packed full of blood corpuscles. The mucous membrane itself is full of small, round cells which stain deeply; these