Atresia of the Esophagus in the Embryo of the Loggerhead Turtle. 357 



is actually the correct interpretation of the significance of the solid 

 esophagus in forms with telolecithal, especially meroblastic, eggs could 

 be definitely established only on the basis of experimental evidence; 

 but lacking such, the available facts speak strongly in favor of such a 

 view. In forms with meiolecithal eggs such a protective mechanism 

 against gut-yolk is superfluous; and it is apparently lacking except in 

 slight and variable degree. A congenital atretic esophagus in mammals 

 could be explained in terms of the persistence or exaggeration of a 

 normal or anomalous embryonic condition, the ontogenetic expression 

 of a phylogenetic experience. 



As already described, the obliteration of the esophageal lumen 

 (contrary to Kreuter) is only partly the result of excessive cell pro- 

 liferation, this being limited to the dorsal wall. The chief factor is 

 a change in form of the cylindric tube, effected by the growth of the 

 esophagus operating against the confining plates of denser mesenchyme, 

 which brings about the separation of the ventral portion of the original 

 esophageo-tracheal anlage to form the laryngo-tracheal tube. The 

 thickened dorsal and the ventral walls of the esophagus are thus 

 brought into apposition and finally fuse, thus obliterating the lumen 

 by a central syncytium. 



Contrary to what one might expect a priori, the lumen of the 

 esophagus is reestablished without any tissue degeneration. This 

 statement is in agreement with the observations both of Kreuter and of 

 Lewis for human embryos. Lewis believes that the constricted lumen 

 of the esophagus in the human embryo becomes enlarged by a process 

 involving a shifting of mitotic activity from the central layer of cells 

 to the peripheral layers, with vacuoles forming as incidental inter- 

 mediate phenomena. In the Caretta embryo there appears no striking 

 evidence to indicate that such a process enters as a large factor. It 

 is true that in the stages preceding the atresia mitotic figures are most 

 numerous centrally, and again that during the reopening of the lumen 

 mitosis is extensive among the peripheral cells; but mitosis is by no 

 means limited to these regions, and the relatively slight excess in one 

 region or the other at the different periods seems to me quite insufficient 

 to account for the early closure and the later vacuolization of the 

 esophagus in the Caretta embryo. 



The chief factor in the closing process is the change in shape of the 

 lumen, which brings the dorsal and ventral walls into contact and 

 results in a fusion. And the main factor in producing the early 

 vacuolization would seem to be the collection of fluid in the ''inter- 

 cellular" spaces of the central syncytial mass. The earlier vacuoles 

 are uniformly spherical and the cells are arranged about them in the 

 manner of an epithelium, such as would result if drops of fluid grew 

 in size among compacted cells. The irregular condition of the later 

 vacuolization indicates, however, that another factor now becomes 



