THE PLACENTA AS AN EEDOCRIN ORGAN 657 



by Knapp. From this account it is evident that eclampsia was well 

 recognized clinically at the time of Aristotle. Many and varied have 

 heen the guesses advanced since that time as to the origin of the disease. 

 That any endocrin factor is involved is improbable. The evidence by 

 which this improbability is inferred follows. 



Schmorl (a) (b) was the first to discover placenta! detritus in the em- 

 boli found in blood vessels of eclamptics and to attribute the eclampsia to 

 placental interference. This hypothesis, however, resting as it did on a 

 purely mechanical basis, was eventually demonstrated to be untenable. 

 Even previous to Schmorl's discovery, it was becoming more and more 

 evident that eclampsia partakes more of the nature of an intoxication than 

 anything else. With the finding by Delore of a microorganism in the 

 blood and tissues of some eclamptics and the apparent confirmation of 

 the observation by Blanc, the idea of a bacterial septicemia being the 

 cause was but natural ; but from the work of Prutz and the discovery by 

 Hofmeister that the supposedly specific organism was none other than 

 proteus vulgaris, the specific causative effect of bacteria was rendered im- 

 probable. Bouchard and Riviere defined eclampsia as an anto-intoxica- 

 tion, while Ludwig and Savor ascribed the toxic influence to the inter- 

 mediary metabolic products. The source of these intermediary products 

 was attributed to the fetus by Van der Hoeven and Fehling, although 

 ffitschmann claimed to be able to disprove the findings. Albeck and, 

 Lohse reported that the injection of amniotic fluid obtained from eclamp- 

 tics into normal animals produced in them all the symptoms of eclampsia. 

 This has, however, yet to be confirmed. 



The trend of opinion and evidence now wandered away from the 

 simpler metabolic by-products into the realm of the more complex sub- 

 stances when Kollmann and others apparently found moTe globulin in 

 the blood of women in normal pregnancies than in that of eclamptics. 

 Sjili and Dienst evolved the "fibrin theory," based in part on the frequent 

 presence of thromboses in eclampsia, and in part on the work of Nasse. 

 This theory was also based partly on ideas of intoxication from fetal 

 by-products, inasmuch as Dienst considered that in eclampsia there is a 

 regressive protein metamorphosis in the fetus which cannot of its chemo- 

 taxic ability cause a real increase in leukocytes in the maternal blood 

 with consequent increase in fibrin precursors. That the placenta might 

 be the seat of the changes causing the intoxication was brought out by 

 Czempin, who held that through malfunctioning of this organ, either as a 

 perversion or as a diminution of functional ability, the fetal by-products 

 are not adequately dealt with and eclampsia results. From the published 

 observations of Pels-Leusden and Schmorl attention was drawn to the 

 possibility that disturbances in syncytial function could well explain the 

 eclamptic phenomena. Using this as a basis, Veit enlarged the idea to 

 the conception that the cause of eclampsia is the giving off from the 





