the lungs of children and in highly pigmented lungs. The capillaries of the pulmonary artery, surrounding the alveoli, anastomose more or less freely with the capillaries of the bronchial artery.

Normally, the alveoli contain air since the very first inspiration after birth; under pathologic conditions, however, the air may be pressed out either through sinking together of the alveolar walls, which come in contact with each other, or by other substances that completely fill the lumen of the alveoli. The first condition is designated as atelectasis. Its prototype is present physiologically during fetal life. In the fetus no air enters the alveoli; they are not expanded, but lie close together; at this time the alveolar epithelium has nuclei, and the flat, thin, nonnucleated platelets are as yet absent. (Plate 31, Fig. I.) Microscopically, the organ shows a compact appearance. The few spaces present correspond to the lumens of the bronchi and bronchioles, while the infundibula are hardly to be made out.

Under various pathologic conditions part of the whole organ may present the same appearance as during fetal life. This is frequently the case when a part or the whole of a lobe is pressed upon, as by tumors, exudates, transudates, by the enlargement of neighboring organs, etc. The lower sharp borders of the lower lobes frequently become compressed and airless as the result of a high position of the diaphragm. Such conditions are designated as compression atelectasis, in contradistinction to resorption or collapse atelectasis, which is also frequent and due to the occlusion of a larger bronchial stem by foreign bodies, mucus, etc., when the air present in the affected district is gradually absorbed. In consequence, the alveoli collapse because no longer exposed to the pressure of the air, and the alveolar lumens become obliterated.

When sections of this kind are stained to bring out

PLATE 31.

FIG. I.-Fetal Atelectasis of Lung. 70. The alveolar walls are very close together, the alveoli not expanded. The tissue, therefore, appears more cellular than normal, aerated, lung tissue. 1, Bronchioles; 2, infundibula; 3, pleura.

FIG. II. Compression Atelectasis of the Lung in Sero= fibrinous Pleuritis. 70. The elastic fibers stained. The alveolar walls with their elastic fibers are approximated and compressed, especially at the peripheral portions. 1, Thickened pleura as a result of inflammation.

the elastic elements, the elastic fibers of the alveolar walls and the walls themselves will be found wrinkled or crumpled and in close contact with each other. (Plate 31, Fig. II.) In compression atelectasis the capillaries, in contrast to fetal atelectasis, are mostly empty and hardly visible; while in resorption atelectasis they usually contain the same amount of blood, if not more, than the surrounding vessels. If the cause in either compression or resorption atelectasis is removed in a certain length of time, it is possible for the affected lung area to return to its normal state. The air-cells become inflated, and their walls are smoothed out. If, however, the condition of atelectasis is present for a longer time, then adhesions take place between the folded alveolar septa. First, the alveolar epithelium degenerates, and then the fixed, connective-tissue cells proliferate, and finally lead to the formation of a cicatricial area which remains permanently airless. When the atelectatic area is located at the periphery of the lung, the pleural or subpleural connective tissue takes an active part in the proliferation and formation of the new tissue. The capillaries are frequently in a state of hyperemia and stasis; they may rupture and lead to extravasations into the thickened tissue, with subsequent deposit of pigments.

Resorption atelectasis, when resulting from bronchitis.