E X P E R I M E N T S ON EMBRYONIC AORTIC ARCHES 357
through the as yet unclosed ventricular septum. In consequence, the
fusion of its components, i.e., the right and left proximal bulbar cushions
and the tubercles from the fused atrioventricular cushions, was disturbed by the blood stream and was not completed, as it is in normal
development, by the 7th day of incubation at the latest (Rychter, 1959).
Tracing the development of these experimental septal defects from
the stage of 5 days 8 hr of incubation (Rychter and Lemez, 1959a), it
was found that the position as well as the form in both types of defect
(disregarding the opposite direction of the blood flow) was the same on
the 6th day of incubation (Fig. 26c, c'). Nevertheless, the two types
could be distinguished by the difference in appearance of the septal
portion of the distal ventral bulbar cushion: in Fig. 26c the cushion was
convex, protruding slightly into the pulmonary part of the heart bulb
(decreased blood output from the right ventricle), while in Fig. 26c' the
cushion was concave (in accordance with the increased blood output
from the right ventricle). About the 7th day of incubation the defects
clearly differed in form and began to move into their definitive subaortic location (Fig. 26d, e) or subpulmonary location (Fig. 26d', e').
The former defects are either triangular, infundibular or semilunar in
form, while the latter defects look like an elongated drop of fluid with
the slit-like end reaching (when at maximal extension) the level of the
pulmonary valves. The distance from the right atrio ventricular orifice
is larger in subpulmonary defects than it is in subaortic defects. The
successive changes in form and location are undoubtedly caused by
haemodynamic differences in the two types.
The ventricular defects occurring irregularly after other experimental
interventions have already been discussed (Section II, B, 2). The defects
varied greatly in size and slightly in form within the limits of the
subaortic and subpulmonary location.
Generally speaking every disturbance of the haemodynamic equilibrium, even though only temporary, may cause a ventricular septal
defect. This has been seen in embryos in which the clip did not eliminate
the intended aortic arch or arches completely, producing only transitory
stenosis.
Further septal defects have been observed in other experiments, viz.,
after suppression of a developing atrium or after retarded morphogenetic
movement of the heart bulb (see Section III, C, D).
B. Experimental Heart Ectopia
Microsurgical experiments on the heart loop cannot avoid a tearing
of the pericardium and of the thin body wall. A small tear heals perfectly, while a larger one frequently causes heart ectopia of various
types.
through the as yet unclosed ventricular septum. In consequence, the
fusion of its components, i.e., the right and left proximal bulbar cushions
and the tubercles from the fused atrioventricular cushions, was disturbed by the blood stream and was not completed, as it is in normal
development, by the 7th day of incubation at the latest (Rychter, 1959).
Tracing the development of these experimental septal defects from
the stage of 5 days 8 hr of incubation (Rychter and Lemez, 1959a), it
was found that the position as well as the form in both types of defect
(disregarding the opposite direction of the blood flow) was the same on
the 6th day of incubation (Fig. 26c, c'). Nevertheless, the two types
could be distinguished by the difference in appearance of the septal
portion of the distal ventral bulbar cushion: in Fig. 26c the cushion was
convex, protruding slightly into the pulmonary part of the heart bulb
(decreased blood output from the right ventricle), while in Fig. 26c' the
cushion was concave (in accordance with the increased blood output
from the right ventricle). About the 7th day of incubation the defects
clearly differed in form and began to move into their definitive subaortic location (Fig. 26d, e) or subpulmonary location (Fig. 26d', e').
The former defects are either triangular, infundibular or semilunar in
form, while the latter defects look like an elongated drop of fluid with
the slit-like end reaching (when at maximal extension) the level of the
pulmonary valves. The distance from the right atrio ventricular orifice
is larger in subpulmonary defects than it is in subaortic defects. The
successive changes in form and location are undoubtedly caused by
haemodynamic differences in the two types.
The ventricular defects occurring irregularly after other experimental
interventions have already been discussed (Section II, B, 2). The defects
varied greatly in size and slightly in form within the limits of the
subaortic and subpulmonary location.
Generally speaking every disturbance of the haemodynamic equilibrium, even though only temporary, may cause a ventricular septal
defect. This has been seen in embryos in which the clip did not eliminate
the intended aortic arch or arches completely, producing only transitory
stenosis.
Further septal defects have been observed in other experiments, viz.,
after suppression of a developing atrium or after retarded morphogenetic
movement of the heart bulb (see Section III, C, D).
B. Experimental Heart Ectopia
Microsurgical experiments on the heart loop cannot avoid a tearing
of the pericardium and of the thin body wall. A small tear heals perfectly, while a larger one frequently causes heart ectopia of various
types.