THE INCREASED knowledge of pulmonary physiology gained through research stimulated by the war, and the extraordinary advance in thoracic surgery in the past few years, have made necessary a critical review of ideas concerning pulmonary pathology as revealed in roentgenograms of the chest. In any such reevaluation, it becomes apparent that there is a scarcity of information relative to diseases of the peripheral vascular system of the lungs, particularly in the radiologic literature. From the standpoint of pathologic classification (1) the small blood vessels of the lung may be affected by disease in a manner which results in increased permeability of their walls, which mayor may not be associated with actual anatomical defects; or in acute or progressive obstruction of their lumina leading to a marked reduction in the pulmonary vascular bed (Table I). This paper deals with the first of these two alternatives. Etiology and Pathology General Considerations Some of the factors associated with damage of the walls of the peripheral vascular system of the lungs may now be considered. It has long been known that the force of a blow may be transmitted through the intact chest wall and produce damage to pulmonary blood vessels, resulting in an outpouring of serum, plasma, or whole blood into the pulmonary tissues. If the trauma is the result of a direct blow, the process in the lungs is localized to a segment or lobe, but the entire substance of both lungs may be affected by the pressure wave of a high explosive blast, without any injury occurring to the thoracic cage. There are two ways in which extravasation of blood elements may be brought about. The direct result of the force applied to the vessel walls may produce changes in tone of capillaries and arterioles, with dilatation and increased permeability, first to fluid, and later to cellular elements; or there may be actual rupture of the vessel wall. On the other hand, the blow may be followed by prolonged arteriolar spasm which markedly decreases the available vascular bed, increases pressure in the pulmonary circuit, and may result in failure of the right ventricle and diffuse pulmonary edema (2). Another possible factor involved in altered function of capillary walls is the presence of a nutritional deficiency state. It has been shown that chronic hypoproteinemia results in latent or obvious anasarca (3) in which pulmonary capillaries may well participate (4). Again, the extent and degree of edema associated with beriberi are often not explained on the basis of cardiac failure alone and Weiss (5) has described the disease as affecting the circulatory system as a whole. There may be episodes of sudden occurrence of a shock-like state which indicates that peripheral vessels, particularly capillaries, may be involved.