260 DISTURBANCES OF CIRCULATION 



of a secondary anemia, without the chemical changes of either 

 leukemia or pernicious anemia. There seems to have been little 

 study of the chemical processes of this disease. Moraczewski l 

 reports a study of metabolism in one case, which showed some 

 retention of nitrogen and calcium, with little change in the phos- 

 phorus and purin bases in the urine. 



HYPEREMIA 

 ACTIVE HYPEREMIA 



This condition is associated with but few chemical changes. 

 Certain chemicals may cause active hyperemia ; some locally, as 

 in the case of irritants, such as alcohol, ether, ammonia, mus- 

 tard, etc., which act either by producing a local vasodilator 

 stimulus or by paralyzing the vasoconstrictors. Other sub- 

 stances may produce active hyperemia in special vascular areas, 

 e. g., cantharides causes active hyperemia in the kidneys, prob- 

 ably because of its elimination through these organs ; pilocarpin 

 causes active hyperemia in the salivary glands and skin, which 

 is associated with increased function. In general, functional 

 activity is associated with active hyperemia, and Gaskell 2 has 

 suggested that this is due to atonicity of the vascular muscle, 

 the result of decreased alkalinity of the lymph flowing away 

 from the active organ along the vessel-walls, it having been 

 found that alkalies cause a tonic contraction and acids an 

 atonic dilatation of arterial muscle. 



Pathological active hyperemia is seldom of long enough dura- 

 tion to lead to any alterations in the tissues in which it occurs. 

 The blood itself remains unchanged, except that the venous 

 blood going from the part contains much less CO 2 and more 

 oxygen than usual, because more oxygen is brought to the 

 tissues than can be used. 



PASSIVE HYPEREMIA 



Passive hyperemia is almost equally unassociated with chem- 

 ical changes, especially in its etiology, which depends almost 

 solely upon mechanical factors. Some chemical alterations 

 result, however, from the changes in the stagnating blood, which 

 may, if the obstruction to outflow is severe, become of venous 

 character in the capillaries of the congested area. Oxidation 

 in the tissues is, therefore, impaired, and some fatty changes may 

 result, e. g., in the center of congested liver lobules. Waste 



1 Virchow's Arch., 1898 (151), 22. 



2 Quoted by Lazarus-Barlow, " Manual of General Pathology," 1904, p. 126. 



