STRUCTURAL CHANGES DUE TO DAMAGE. 



327 



in less degree. This contraction would suffice to compromise at 

 least the smaller branches of the portal vein entering the lobules, 

 so as to obstruct the current of blood flowing through them. The 

 result is an increase of pressure in the portal circulation and the 

 production of passive hyperaemia or congestion of the organs in 

 which the portal radicles are situated. 



This passive congestion results in a dilatation of the vessels in 



FIG. 289. 



Brown induration of the lung, the result of chronic passive congestion caused by valvular 

 disease of the heart : a, small radicle of the pulmonary vein, dilated and filled with 

 blood ; 6, alveolar wall in cross-section, thickened and containing an abnormal number 

 of nuclei (evidence of an increase of tissue, a chronic interstitial pneumonia) ; e, surface- 

 view of an alveolar wall, showing similar abundance of nuclei and a dilatation of the 

 capillaries, evidenced here and elsewhere in the section by a double row of corpuscles in 

 a capillary ; d, cavity of an alveolus ; e, alveolus containing serum, red corpuscles, and 

 leucocytes, and also large pigmented cells. These are chiefly leucocytes which have 

 taken up pigment from the red corpuscles that have disintegrated phagocytes. Some 

 of these large cells may be desquamated epithelial cells from the alveolar walls, in 

 a swollen and degenerated condition. The presence of serum is demonstrated by the 

 fact that the cells in the alveolus are not lying against the alveolar walls. The escape 

 of the blood-corpuscles from the capillaries is a result of the sluggish circulation. 



those organs and a thickening of their walls, and also frequently 

 induces a chronic interstitial inflammation. It may also so impede 

 the lymphatic circulation and impair the nutrition of the vascular 



