THE LIVER AND BLOOD PIGMENTS. 335 



that it must undergo a secondary process in the liver before 

 it can serve its physiological purpose in the arterial circula- 

 tion. This is sustained by the prevailing view as to the func- 

 tions of the spleen, i.e., that it disintegrates worn-out red 

 corpuscles, and also by the great increase of leucocytes ob- 

 served in the splenic vein as compared to the proportion of 

 these cells in the artery. It therefore seems logical to conclude 

 that both in the lymphatic structures of the intestine and in those 

 of the spleen leucocytes are formed which carry iron-pigments to 

 the portal vein; those from the intestine reach the latter by the 

 superior mesenteric vein, and those from the spleen by the splenic 

 vein. As Macallum observed iron-pigment leucocytes in the 

 spleen similar to those witnessed in the intestinal villi, and the 

 venules of the latter and the splenic vein ultimately transmit- 

 ting their blood to the portal vein, no other conclusion seems 

 possible. 



The similarity of the general mechanism involved suggests 

 the presence of correlated functions. Thus, in the spleen the 

 leucocytes are formed in situ, pass out into the pulp-channels, and 

 take up the iron-pigment and carry it out to the liver; in the 

 intestine they are formed in a similar structure, the follicle, 

 pass out into the intestinal channel, take on a similar supply of 

 blood-pigment, re-enter through the villi into the venous system, 

 and also proceed to the liver. True, we have previously ascribed 

 bactericidal properties to the leucocytes produced by the intes- 

 tinal follicles; but the chemotactic property of the leucocytes, 

 the existence of which is shown by their ability to take up the 

 pigments, serves but to demonstrate that they must also be 

 endowed at least with phagocytic attributes. 



We also ascertained, in the chapter referred to, that, while 

 the adrenals supply an oxidizable substance to the blood, in- 

 sufficiency of the adrenals leads to the formation of a com- 

 pound inferior to haemoglobin in oxygen-absorbing powers, 

 i.e., methaemoglobin; and, furthermore, that haamatoporphyrin 

 is formed when the suprarenal insufficiency is still further ad- 

 vanced, haemoglobin being unable to hold itself together, as it 

 were, and to absorb oxygen. Again, we saw that haemoglobin 

 is reduced to haematin when the reaction with the reducing 

 agent occurs in the presence of oxygen. In the absence of oxygen 



