678 CHARLES W. HOOPER 



hemoglobin and to the hematogenous jaundice produced by chloroform 

 anesthesia. In 1917 they found that the Eck fistula liver secretes from 

 one- third to three-fourths the normal amount of bile pigment. Splenec- 

 tomy added to the combined bile and Eck fistula does not essentially mod- 

 ify the result. Also, they have found that the simple bile fistula and the 

 combined bile and Eck fistula dogs show the same histological picture in 

 the hematopoietic system. This indicates that bile pigment formation is 

 in part dependent upon liver function and not solely upon red cell dis- 

 integration. Possibly the production of hemoglobin may depend in part 

 upon the constructive capacity of the liver. Hooper and Whipple (c) 

 (1917) reported experiments which show that the Eck fistula liver can 

 eliminate hemoglobin from the blood stream as promptly as the control 

 liver. Even with a high red count the color index will often be low in the 

 Eck fistula. This is evidence that the Eck fistula animal has a subnormal 

 pigment building capacity. The Eck fistula dogs show periods of anemia, 

 which may be referable to an inadequate supply of prepigment material 

 manufactured in the liver. The anemia after bleeding is much more severe 

 and the following period of blood regeneration is much longer than that of 

 normal dogs. Combined Eck and bile fistula dogs show less tendency to 

 develop icterus with bile pigments in the urine than do the simple bile 

 fistula dogs. Apparently the Eck fistula liver can excrete the pigment 

 radical of hemoglobin as promptly as the normal liver. Bile pigment and 

 hemoglobin formation can be controlled at will by diet. These facts over- 

 throw the long accepted theory that bile pigment is formed only as the 

 result of the disintegration of red cells ; and they furnish direct evidence 

 that the liver may construct a prepigment material which may be utilized 

 as a true internal secretion to construct prehemoglobm and hemoglobin as 

 needed by the red cells, while the excess reserve supply which is not needed 

 in the body economy is excreted in the bile as bile pigments. 



Blood Serum Proteins as Hepatic Internal Secretions 



Origin of Blood Serum Proteins. Seitz (1906) stated that the liver 

 may act as a storehouse for serum proteins. Grenet (1907) and Gilbert and 

 Chiray (1907) found the serum proteins decreased in clinical cases of 

 liver insufficiency. Kerr, Hurwitz and Whipple (1918) presented experi- 

 mental evidence that the liver may be concerned in maintaining the normal 

 level of the blood serum proteins. Eck fistula dogs show a distinct inability 

 to regenerate blood serum proteins following plasma depletion. Pro- 

 nounced injury of the liver by means of phosphorus or chloroform will be 

 associated with moderate fall in blood serum proteins. Regeneration of 

 blood serum proteins following plasma depletion will be delayed by the 

 presence of liver injury. These experiments indicate that liver insuffi- 



