esophagus, atresia, respiratory, normal and anlage

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(5) The esophageal atresia involves also a transient stenosis and atresia of the oral end (glottis) of the respiratory anlage.

(6) The definitive perforate esophagus becomes established by a process involving the transformation of certain "intercellular" spaces in the central syncytium into spherical vacuoles, and the enlargement and confluence of these to form larger irregular areolie; at this stage (32-day) the relatively wide esophageal lumen is spanned by delicate nucleated septa; these septa are ultimately drawn into the expanding peripheral wall and here incorporated with practically no tissue degeneration; the earlier spherical shape of the vacuoles and the dis position of the nuclei around these spaces indicate their formation under the influence of an internal fluid pressure, but no coagulum appears in fixed and stained tissues; the processes of later vacuolization and incorporation of the intra-luminal septa by the peripheral wall are probably largely the results of the growth expansion of the eso phageal tube resulting from active proliferation of the lining-cells and assisted by the now very loose and vascular enveloping mesenchyme, the primitive submucosa of the esophagus.

(7) The lumen of the esophagus is still occluded just behind the laryngeal orifice at the 32-day stage and no doubt remains stenosed until near the close of the incubation period (56 days).

(8) All forms in which an extensive atresia of the esophagus has been reported (elasmobranchii, bony fishes, amphibians, certain rep tiles, chick) have the gut open to a huge yolk-sac during the greater portion of the incubation period.

The above-enumerated facts would seem to show conclusively that in the Caretta embryo the temporary atresia of the esophagus is a normal phase of the developmental process. This is probably true also of all forms with large yolk-sacs. The occasional esophageal constrictions, stenoses, and atresias in the pig embryo, other mamma lian embryos, and in man (a normal phenomenon according to Kreuter, abnormal according to Lewis) probably have their explanation in terms of their reptilian ancestry. These conditions in mammals are apparently very variable and any discussion as to their normality or abnormality in these embryos seems of small value. Congenital stenoses or atresias of the esophagus in humans, as Kreuter has already suggested, represent most likely a persistence or exaggeration of a normal phase of embryonic development.

A suggestion of the teleological significance of this temporary atresia of the esophagus in Caretta may be obtained by seeking to disclose what is actually accomplished by the phenomenon. Ob viously, it closes the respiratory anlage against the more solid contents of the gut during the greater portion of the incubation period. That the relation of the obliteration of the lumen of the esophagus is close to the development of the respiratory anlage is strongly indicated by the following facts: (1) Its first appearance about the time the laryngo-tracheal groove begins to be separated from the esophagus and at or just behind the later orifice of the larynx.

(2) The extension of the atresia even into the glottis.

(3) The persistence of the atresia orally until nearly the end of the incubation period, when the lung is already greatly developed, and the yolk is almost entirely digested.

It is difficult to avoid the inference that the temporary solidification of the esophagus is a device to protect the developing lung against the invasion from the gut of yolk-globules. The respiratory anlage, being a derivative of the primitive esophagus, is originally lined by an epithe lium which retains in part the ability to digest yolk material; but soon after, as it becomes more and more differentiated into the respiratory type of entodermal epithelium, it must more and more lose the capacity for digesting crude yolk material. It seems reasonable to suppose that large quantities of yolk-globules within the pulmonary anlages would seriously interfere with their normal development. That this 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 alight 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.

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