538 XI. HEMOGLOBIN CATABOLISM, I 



breakdown, although even this has been doubted (675, 2241, 28U)- Vahl- 

 quist {3844-) found a decrease, not an increase, of plasma iron after birth 

 {cf. Section lO.S.^.) and concludes that there is no reliable evidence for 

 increased blood destruction. Several workers (Wintrobe, 3104,3106\ Sachs 

 and co-workers, 2407) were unable to find a true polycythemia. Wintrobe 

 found only macrocytosis which he explains as due to the belated appearance 

 of the antipernicious anemia principle. Sachs and co-workers found the cell 

 count increased in the peripheral, not in the cord, blood, while others found 

 no polycythemia in infants delivered by Caesarean section. They assume 

 that the polycythemia is caused by traumatic shock at birth. The maximum 

 of the polycythemia occurs, indeed, 48 hours after birth (30,919). Poly- 

 cythemia has, however, also been observed in hatching chicks {1326; cf. 

 2017, p. 648), in which the explanation in terms of a traumatic shock is 

 unlikely. 



Another point which is still unsettled is the storage of iron in the liver of 

 the fetus. While the nonhematin iron content of the fetal liver has been 

 found to be higher than that of the adult liver by many workers, others have 

 been unable to confirm this {cf. the discussion by Needham, 2017, p. 651; 

 and,36i). 



The polycythemia of the newborn has been explained as an adaptation 

 to the life of the fetus at low oxygen pressures (Anselmino and Hoffmann, 

 69-62; cf. also 1015;2017, p. 648) or as adaptation to the poor iron supply 

 in the milk (Bunge, Abderhalden), but in view of the uncertainty of the 

 experimental findings a discussion appears unprofitable. 



7. SITE OF BILE PIGMENT FORMATION 

 7.1. The Reticuloendothelial System 



In Section 5. the main emphasis has been on the factors leading to 

 the disintegration of the corpuscle. The amount of hemoglobin 

 destroyed within the corpuscle during the normal breakdown amounts 

 only to about 10% of the daily breakdown, the remaining 90% being 

 transformed to bile pigment elsewhere. The site of this breakdown 

 must now be discussed. 



In 1886 Minkowski and Naunyn {1959) observed that arsine no 

 longer produced a marked jaundice in geese after hepatectomy. 

 They concluded that bilirubin is formed in the epithelial cells of the 

 liver. This theory has been superseded by that of Lowit {1773), 

 McNee {1843), Eppinger {697), Lepehne {1717), and Aschoff {85-88) 

 {cf. the review of Rich, 2240), according to which bile pigment is 

 formed in the cells of the reticuloendothelial system. This system 

 consists of a widely distributed variety of cells of mesenchymic 

 origin which possess phagocytic properties and are able to change 

 readily from a sessile to an amoeboid state and back again. Such 



