E X P E R I M E N T S ON EMBRYONIC AORTIC ARCHES 367
deduce from morphological anomalies the time when the malformations
"originated" '.
V. Theory of the Teratogenetic Meaning of Local Damage to the
Heart Loop and Aortic Arches
It is now possible to discuss our results and the theory derived from
them with regard to the place they occupy in the realm of present
research on congenital malformation.
It would be naive to suppose that the silver clip, that is, external
mechanical compression, truly represents any naturally occurring
teratogenetic factor. If for instance the 6th or 4th aortic arch were
suppressed on the 4th or on the 3rd day of incubation, or even prior to
the formation of the vessel in the corresponding branchial arch (Rychter,
unpublished data), the result has always been the same. This means that
the clip served as an unspecific factor (in most cases the clip left the
embryonic body spontaneously after 48 hr) evoking a model agenesis of
the aortic arch. The consequences of this model malformation always
occurred and were governed by rules and causal relations set out in the
series of papers discussed. The same was true for the transposition of the
aorta into the right ventricle, where after 48 hr of further incubation the
rhombic clip was removed: the malformation developed in practically
all cases. Likewise after the suppression of the developing left atrium a
series of alterations necessarily followed, starting with the stenosis of the
left atrioventricular orifice and ending with the stenosis of the corresponding great arterial stem. Such a hypoplasia of the left atrium has
been described in spontaneously occurring malformation as a consequence of a too small foramen ovale. In a broader sense this series
demonstrates part of the string of events which are latent in the
developing embryo and which interfere with normal development at a
certain point and result in a morphological manifestation of the
malformation concerned. This string of events ('deviation of developmental processes into abnormal channels', Gluecksohn-Waelsch,
1957; 'embryonic channel', Grüneberg, 1960; 'morphologic pathways',
Nelson, 1960) could best be analysed by means of the technique of a
directed local intervention. It depends on the nature of the experimental
technique at which point the channel will be entered. It is apparent that
the longest channels belong to the genetically caused malformations.
According to Nelson (1960) the number of morphologic pathways in the
embryo seems to be limited, which agrees with our findings on the
heart loop.
The results of experimentally produced model malformations of the
heart and aortic arches have made it possible to analyse the develop-
deduce from morphological anomalies the time when the malformations
"originated" '.
V. Theory of the Teratogenetic Meaning of Local Damage to the
Heart Loop and Aortic Arches
It is now possible to discuss our results and the theory derived from
them with regard to the place they occupy in the realm of present
research on congenital malformation.
It would be naive to suppose that the silver clip, that is, external
mechanical compression, truly represents any naturally occurring
teratogenetic factor. If for instance the 6th or 4th aortic arch were
suppressed on the 4th or on the 3rd day of incubation, or even prior to
the formation of the vessel in the corresponding branchial arch (Rychter,
unpublished data), the result has always been the same. This means that
the clip served as an unspecific factor (in most cases the clip left the
embryonic body spontaneously after 48 hr) evoking a model agenesis of
the aortic arch. The consequences of this model malformation always
occurred and were governed by rules and causal relations set out in the
series of papers discussed. The same was true for the transposition of the
aorta into the right ventricle, where after 48 hr of further incubation the
rhombic clip was removed: the malformation developed in practically
all cases. Likewise after the suppression of the developing left atrium a
series of alterations necessarily followed, starting with the stenosis of the
left atrioventricular orifice and ending with the stenosis of the corresponding great arterial stem. Such a hypoplasia of the left atrium has
been described in spontaneously occurring malformation as a consequence of a too small foramen ovale. In a broader sense this series
demonstrates part of the string of events which are latent in the
developing embryo and which interfere with normal development at a
certain point and result in a morphological manifestation of the
malformation concerned. This string of events ('deviation of developmental processes into abnormal channels', Gluecksohn-Waelsch,
1957; 'embryonic channel', Grüneberg, 1960; 'morphologic pathways',
Nelson, 1960) could best be analysed by means of the technique of a
directed local intervention. It depends on the nature of the experimental
technique at which point the channel will be entered. It is apparent that
the longest channels belong to the genetically caused malformations.
According to Nelson (1960) the number of morphologic pathways in the
embryo seems to be limited, which agrees with our findings on the
heart loop.
The results of experimentally produced model malformations of the
heart and aortic arches have made it possible to analyse the develop-