AORTIC-ARCH SYSTEM IN THE HUMAN EMBRYO. 65 



to the retraction of its mesenchymal sheath (plate 3, figs. 37 to 39) . The endothelial 

 core was traced backward through a few sections as a solid rod. The anterior end 

 of the degenerating vessel was not found. 



If tension in connection with the caudal shifting of the aorta plays a causal role 

 in the disruption of the pair of aortic segments, it seems to be secondary in impor- 

 tance to a decrease in the current-flow. The contrasting curves of the third and 

 fourth arches, before the segment has stretched perceptibly, indicate that the cur- 

 rent is passing from them to the aorta in opposite directions, and consequently the 

 stream in the disappearing segment is nearly at a standstill. 



The interruption of the caudal part of the right paired aorta takes place in a 

 manner very different from that indicated by current figures and descriptions. 

 These err in representing the obliteration of a long segment of the vessel. There is, 

 in fact, great economy of material in this operation, since only an insignificant ter- 

 minal segment actually disappears. Before it has been especially affected, the entire 

 right paired aorta, as far forward as the fourth arch, becomes reduced in diameter, so 

 that it retains a lumen adequate only for the supply of the subclavian. Decrease in 

 current here seems to be the primary cause of involution, as in the case of the pul- 

 monary arch. Here, also, the left counterpart persists, having a larger current. 

 The cause of the falling off of the current of the right vessel relative to the left is 

 probably to be found in changes that have come about in the pulmonary aortic 

 trunks at this time. As has already been explained, the pulmonary trunk is now 

 throwing its current entirely into the left paired aorta. The aortic trunk also, in the 

 two embryos that were studied, has taken an oblique direction, well marked later, 

 and is therefore sending more blood into the left than into the right fourth arch. The 

 greater part of the right paired aorta caudal to the fourth arch retains a diameter 

 equal to the subclavian. The short caudal end distal to the subclavian shows further 

 contraction by a narrowing of its lumen and a thickening of its wall. Later, as the 

 aorta shifts caudally, it is stretched out into a filament over 3 vertebral segments in 

 length (fig. 14). This is made possible by the fixation of the more caudal part of the 

 paired aorta by the right subclavian and its branch, the vertebral, which thus 

 fastens it to the vertebral column and to the surrounding tissues. 



The different interruptions here described seem to have much in common and 

 are due to the same factors that brought about the involution of the first and second 

 arches. In each instance there is a preliminary decrease of current-flow, though its 

 cause in the unpaired and symmetrical segments is dissimilar. It seems probable 

 that longitudinal tension, resulting from the caudal shifting of the heart and aorta, 

 serves to augment the effect of the change in current. At an early stage there is 

 lacking clear proof of tension, such as would be furnished in the case of a stretched 

 rubber tube by the narrowing of its wall and lumen. The first decrease in caliber 

 was due to a contraction of the vessels and was therefore accompanied by a thick- 

 ening of the wall. The response of the artery to the tension and other unfavorable 

 influences was vital in its nature and not merely physical. It was only after their 

 walls weakened that the aortic segments were rapidly pulled out into filaments. The 

 pressure of the vagus nerve probably assisted in the involution of the left pulmonary 



