E X P E R I M E N T S ON EMBRYONIC AORTIC ARCHES 359
left atrium remained highly hypoplastic (Fig. 21b', d') or was absent
altogether; the left ventricle was hypoplastic as well and the ventricular outlet was somewhat narrowed. The most conspicuous feature
was the marked narrowing of the arcus aortae (Fig. 27b', d') behind the
beginning of the brachiocephalic trunks, which were of normal size.
If the left atrium (from the ventral aspect) was one-fourth or less the
size of the right, then the arcus aortae was completely atretic or even
interrupted in its distal portion. According to the usage of human
pathology a coarctation of the aorta (disregarding the difference in
aortic arch pattern of birds and mammals) was accomplished by the
experiment. The new haemodynamic approach to the problem of
coarctation of the aorta has the advantage of being the result of experiment and not an observation of an already full developed malformation,
in which the cause cannot be distinguished from an associated phenomenon. Recently, Moffat (1960) attempted to explain the origin of
aortic coarctation in rat embryos from the new standpoint of the
correlative growth of various parts of the arcus aortae influencing the
normal development of the aortic isthmus. The results after suppression
of the right atrium differed from that just described, only in the less
frequent and less conspicuous narrowing of the pulmonary trunk (Fig.
27b, d). In both cases the corresponding atrioventricular orifice was
reduced in size, i.e., stenotic.
After suppression of the left developing atrium, ventricular septal
defects occurred in 25% of the embryos, while intervention on the right
side led to defects in 60%. Though the cause leading to the defects was
undoubtedly a haemodynamic one, no strict correlation between the
defects and aortic or pulmonary stenosis was observed. After suppression
of the left atrium the defect was usually triangular, rather funnel shaped
(Fig. 27c'), and was of subaortic location. According to previous findings
(Section III, A) the blood stream ran from the right ventricle into the
left ventricular outlet. After suppression of the right atrium two types
of ventricular septal defect were observed; they were either of the
subpulmonary type, already described, in various sizes or they were
characterized by a low position in the ventricular septum in the
vicinity of the stenotic right atrioventricular orifice, separated from the
latter by fused hypoplastic tubercles of the atrioventricular cushions
(Fig. 27c-T). The hypoplasia is already expressed on the 6th day of
incubation (Fig. 27, compare b and &'). The difference in size of the two
ventricles is most conspicious in the outline of the heart on the 7th day
of incubation (Fig. 27d, d'); during later development the general shape
of the heart becomes more normal.
It was remarkable that small ventricular septal defects were also
present in those embryos in which recovery from the atrial suppression
left atrium remained highly hypoplastic (Fig. 21b', d') or was absent
altogether; the left ventricle was hypoplastic as well and the ventricular outlet was somewhat narrowed. The most conspicuous feature
was the marked narrowing of the arcus aortae (Fig. 27b', d') behind the
beginning of the brachiocephalic trunks, which were of normal size.
If the left atrium (from the ventral aspect) was one-fourth or less the
size of the right, then the arcus aortae was completely atretic or even
interrupted in its distal portion. According to the usage of human
pathology a coarctation of the aorta (disregarding the difference in
aortic arch pattern of birds and mammals) was accomplished by the
experiment. The new haemodynamic approach to the problem of
coarctation of the aorta has the advantage of being the result of experiment and not an observation of an already full developed malformation,
in which the cause cannot be distinguished from an associated phenomenon. Recently, Moffat (1960) attempted to explain the origin of
aortic coarctation in rat embryos from the new standpoint of the
correlative growth of various parts of the arcus aortae influencing the
normal development of the aortic isthmus. The results after suppression
of the right atrium differed from that just described, only in the less
frequent and less conspicuous narrowing of the pulmonary trunk (Fig.
27b, d). In both cases the corresponding atrioventricular orifice was
reduced in size, i.e., stenotic.
After suppression of the left developing atrium, ventricular septal
defects occurred in 25% of the embryos, while intervention on the right
side led to defects in 60%. Though the cause leading to the defects was
undoubtedly a haemodynamic one, no strict correlation between the
defects and aortic or pulmonary stenosis was observed. After suppression
of the left atrium the defect was usually triangular, rather funnel shaped
(Fig. 27c'), and was of subaortic location. According to previous findings
(Section III, A) the blood stream ran from the right ventricle into the
left ventricular outlet. After suppression of the right atrium two types
of ventricular septal defect were observed; they were either of the
subpulmonary type, already described, in various sizes or they were
characterized by a low position in the ventricular septum in the
vicinity of the stenotic right atrioventricular orifice, separated from the
latter by fused hypoplastic tubercles of the atrioventricular cushions
(Fig. 27c-T). The hypoplasia is already expressed on the 6th day of
incubation (Fig. 27, compare b and &'). The difference in size of the two
ventricles is most conspicious in the outline of the heart on the 7th day
of incubation (Fig. 27d, d'); during later development the general shape
of the heart becomes more normal.
It was remarkable that small ventricular septal defects were also
present in those embryos in which recovery from the atrial suppression