653 



protein in the blood for, as Hoover and Blankenhorn have shown, it is 

 not dialyzable until it can be excreted by the kidneys. In pernicious 

 anemia and lead poisoning these observers have found bile salts in the 

 blood, in the absence of bile pigments. 



In severe and long standing jaundice, especially that due to gall 

 stones, a retention of cholesterol in the blood may result, probably because- 

 it is not excreted in the bile. However, Rothschild and Felsen record low 

 blood cholesterol values in severe jaundice complicating cirrhosis; there- 

 fore, the above simple explanation does not suffice. These authors suggest 

 that a. selective retention of bile pigments may occur while cholesterol is 

 being eliminated in normal or increased amounts. The constitutional 

 symptoms observed in severe jaundice, especially the slow pulse and the 

 low -blood pressure, have been variously ascribed to the action of bile salts 

 and pigments respectively. King and Stewart have observed that the 

 amount of pigment in a lethal dose of bile is sufficient to produce a fall in 

 blood pressure and a slowing of the pulse, whereas the bile salts therein 

 were without effect. When bilirubin was combined with calcium it 

 became ineffective. They conclude that the poisonous effect of bile is due 

 to the withdrawal of active calcium from the blood by bilirubin (King, 

 Bigelow and Pearce). 



Recently Wieland, working with pure salts of cholic and desoxycholic 

 acids, was able to show that the salts of the latter, when perfused through 

 the isolated frog heart, produce a diminution of ventricular contraction 

 and an irregularity of the heart beat even in dilutions of 1 : 12, 800. They 

 also decrease the efficiency of striped muscle and hemolyze red blood cells. 

 When desoxycholic acid was administered subcutaneously, this action on 

 the heart, striped muscle and red blood cells was very much decreased. 

 The salts of desoxycholic acid are not as powerfully hemolytic as sodium 

 oleate, for the latter is active in a dilution of 1 :50,000, while desoxycholic 

 loses its activity in dilutions greater than 1 :1,960 and cholic acid in dilu- 

 tions greater than 1 :220. The absence of bile salts results in a diminished 

 absorption of fats from the intestine. The emaciation often observed in 

 jaundice is probably to be ascribed to the withdrawal of fats from the 

 dietary. The amount of urobilinogen and urobilin in the stool indicates 

 whether the obstruction is complete or partial. The light color of the 

 stools of jaundiced patients is due to the absence of urobilin and in some 

 instances to the presence of increased quantities of fat. 



In catarrhal jaundice, the liver parenchyma is usually affected as 

 shown by the galactose test and the presence of urobilin in the urine, 

 whereas, in occlusion of the common bile duct by tumors, or in experi- 

 mental ligation of the duct, there is no indication of malfunction of the 

 liver. The absence of glycogen from the liver in jaundice has frequently 

 been observed. A decreased formation of urea does not occur. 



Acute Yellow Atrophy. Acute yellow atrophy may be a sequel of 



