360
Z. RYCHTER
had obviously occurred (the trabeculization of the atrial wall was
normal, in contrast to those suppressed atria which were passively
distended and 'smooth'). This means that a merely temporary disturbance of atrial development can change the haemodynamic equilibrium so as to influence the fusion of the ventricular septal components.
Similarly the septal defects were encountered in unsuccessful eliminations of aortic arches.
The present experiments proved that injury to a proximal part of the
heart loop evokes haemodynamic changes in its distal parts also.
Starting with any link in this chain, the distally localized alterations
necessarily appeared. In the case of entire 'right or left heart' hypoplasia
it is not necessary, therefore, to suppose that the right or left heart
anläge was damaged as was suggested by Bredt (1935) and Doerr (1955).
From the standpoint of comparative anatomy, our conclusions seem
to be well supported by the investigations of Noble (1925): a reduction
of the lungs in all amphibia is correlated with a reduction of the left
atrium. An extensive reduction of the lungs such as that found only in
urodeles leads also to fenestration of the atrial septum and to a loss of
the spiral valve in the heart bulb.
D. Transposition of the Aorta into the Right Ventricle
Further experiments were performed by means of a relatively large
rhombic clip placed in the bulboventricular groove (which entirely
disappears during normal development) of the heart loop on the 3rd or
4th day of incubation (Fig. 28a, a') (Rychter and Lemez, 1959b, c;
1960b). After 48 hr of incubation, the rhombic clip must, of course,
be removed or loosened in order to prevent strangulation of the heart
in later development.
Such a clip placed on the heart loop on the 3rd day of incubation
prevents the morphogenetic movement of the heart bulb to the left, so
that the aortic and pulmonary trunks remain in their original spatial
relation to the right ventricle (viz. to the ascending part of the heart
loop) (Fig. 28d). This is already apparent on the 6th day of incubation
(Fig. 28b). The same figure shows that both the proximal and distal
bulbar cushions are still present on the 6th day of incubation, while
during later development the proximal cushion rudiments are only
present as boundaries of the ventricular septal defect (Fig. 28c); of the
distal cushions, only the valvular portions remain, the septal portion
having disappeared. The channel-like shape of the defect in some cases
forces the blood stream into the aortic ostium (in the right ventricle)
so that the transposition is at least partially corrected from a functional
viewpoint (Fig. 28c—arrow).
A similar transposition has been described by Le Douarin (1960)
Z. RYCHTER
had obviously occurred (the trabeculization of the atrial wall was
normal, in contrast to those suppressed atria which were passively
distended and 'smooth'). This means that a merely temporary disturbance of atrial development can change the haemodynamic equilibrium so as to influence the fusion of the ventricular septal components.
Similarly the septal defects were encountered in unsuccessful eliminations of aortic arches.
The present experiments proved that injury to a proximal part of the
heart loop evokes haemodynamic changes in its distal parts also.
Starting with any link in this chain, the distally localized alterations
necessarily appeared. In the case of entire 'right or left heart' hypoplasia
it is not necessary, therefore, to suppose that the right or left heart
anläge was damaged as was suggested by Bredt (1935) and Doerr (1955).
From the standpoint of comparative anatomy, our conclusions seem
to be well supported by the investigations of Noble (1925): a reduction
of the lungs in all amphibia is correlated with a reduction of the left
atrium. An extensive reduction of the lungs such as that found only in
urodeles leads also to fenestration of the atrial septum and to a loss of
the spiral valve in the heart bulb.
D. Transposition of the Aorta into the Right Ventricle
Further experiments were performed by means of a relatively large
rhombic clip placed in the bulboventricular groove (which entirely
disappears during normal development) of the heart loop on the 3rd or
4th day of incubation (Fig. 28a, a') (Rychter and Lemez, 1959b, c;
1960b). After 48 hr of incubation, the rhombic clip must, of course,
be removed or loosened in order to prevent strangulation of the heart
in later development.
Such a clip placed on the heart loop on the 3rd day of incubation
prevents the morphogenetic movement of the heart bulb to the left, so
that the aortic and pulmonary trunks remain in their original spatial
relation to the right ventricle (viz. to the ascending part of the heart
loop) (Fig. 28d). This is already apparent on the 6th day of incubation
(Fig. 28b). The same figure shows that both the proximal and distal
bulbar cushions are still present on the 6th day of incubation, while
during later development the proximal cushion rudiments are only
present as boundaries of the ventricular septal defect (Fig. 28c); of the
distal cushions, only the valvular portions remain, the septal portion
having disappeared. The channel-like shape of the defect in some cases
forces the blood stream into the aortic ostium (in the right ventricle)
so that the transposition is at least partially corrected from a functional
viewpoint (Fig. 28c—arrow).
A similar transposition has been described by Le Douarin (1960)