112 George B. Wislocki 



variously ascribed to a variety of placental lesions. Premature 

 and excessive degeneration of the syncytial trophoblast has 

 been held responsible for these conditions (Tenney, 1936; 

 Tenney and Parker, 1940), and, since the syncytium is re- 

 garded as the site of formation of placental ketosteroids 

 (Wislocki and Bennett, 1943; Wislocki, 1955), the observed 

 changes in ketosteroid metabolism in the toxaemias have been 

 ascribed to syncytial degeneration (Smith and Smith, 1948; 

 Sommerville, 1950). Bartholomew and his associates (1932, 

 1934, 1936) have attributed the toxaemias to spastic constric- 

 tions of the foetal blood vessels of the chorionic villi, resulting 

 in the formation of red infarcts with necrosis of the villi in the 

 infarcted areas. Thomsen (1955) agrees with him, except that 

 he regards the placental lesions as secondary rather than as 

 the primary precipitating cause of eclampsia. Many other 

 speculative explanations of the toxaemias of pregnancy have 

 been advanced (cf. Dieckmann, 1952). Schneider (1950), for 

 example, attributes these conditions to the toxic effects of 

 thromboplastin liberated from pathological haematomas 

 which frequently occur between the decidua and the basal 

 placental plate late in pregnancy. Page (1953) offers a theory 

 involving an unidentified vaso-toxic substance produced in 

 the placenta, combined with a high sodium intake and the 

 presence of large quantities of placental steroids. 



In two cases of pre-eclampsia, Flexner and his associates 

 found a marked reduction in placental permeability to radio- 

 active sodium. In toxaemia the ability of the placenta to con- 

 centrate amino acids is also decreased (Crumpler, Dent and 

 Lindan, 1950; Villee, 1955). 



One avenue of investigation of terminal placental ageing 

 remains to be mentioned, namely, the postmature retention of 

 foetuses in utero induced by inhibition of parturition. This was 

 first accomplished experimentally by producing a fresh set of 

 corpora lutea in the rabbit on the 28th day of pregnancy 

 (Snyder, 1934), and later by others as the result of injecting 

 progesterone. Following this procedure, the foetuses remain 

 alive and continue to grow for 4 to 6 days beyond the normal 



