368
Z. RYCHTER
ment of the hereditary ventricular septal defects occurring in the S-line
of Brown Leghorn chicks (Siller, 1958). By a microdissection method,
various deviations from normal development were encountered
(Rychter, Lemez and Siller, 1960): stenosis of the right atrioventricular
orifice, hypoplasia of the fused tubercles of the right atrio ventricular
orifice, abnormal cushion in the future aortic part of the heart bulb, and
agenesis of the right 4th aortic arch. Could these deviations, which, with
the exception of the missing arcus aortae, were not present after the 7th
day of incubation be the cause of the ventricular septal defect? The
experimentally produced malformation showed that ventricular septal
defects are associated at least to some extent with three of them.
Analysis by means of an injection of a solution of Geigy blue revealed
that the abnormal cushion caused deviation of the coloured blood stream
through the unclosed ventricular septum into the right ventricle and
could, therefore, be considered as a cause of the defect as well. The
observations have demonstrated that a relatively uniform congenital
heart malformation, ventricular septal defect, could have quite different
morphologic pathways of development.
According to a personal communication from Dr. Rychterova (1960)
4 cases of coarctation of the aorta found in human neonates showed a
distinct hypoplasia of the entire left half of the heart, especially of the
left auricle. This demonstrates that the new point of view can be useful
to human pathologists, who are inclined to consider 'left heart' hypoplasia as 'right heart' hypertrophy.
Speaking about 'damage' of the heart loop wall and of the aortic
arches, one must bear in mind that the damage need not necessarily be
of a negative character, but that it can appear as a consequence of local
abundant proliferation (e.g., abnormal bulbar cushion), even though
only temporary.
The teratogenetic critical loci ought not to be analysed merely from
the traditional standpoint of a higher metabolic activity etc., but rather
from the standpoint of their significance in morphogenesis and of their
influence on haemodynamics which conversely act on the morphogenesis of the heart loop and the aortic arches.
It is most probable that a much greater number of embryos are
exposed to 'damage' than would follow from the overall frequency of
cardiovascular malformations: in these embryos the teratogenetic
critical loci were probably not hit and the damage was completely
regulated without leaving manifest alterations. If, however, a teratogenetic critical locus has been hit, then the compensatory, correlative,
and regulative changes would appear controlled by the factors and rules
summarized in the present review.
The solution to the problem of congenital cardiovascular malforma-
Z. RYCHTER
ment of the hereditary ventricular septal defects occurring in the S-line
of Brown Leghorn chicks (Siller, 1958). By a microdissection method,
various deviations from normal development were encountered
(Rychter, Lemez and Siller, 1960): stenosis of the right atrioventricular
orifice, hypoplasia of the fused tubercles of the right atrio ventricular
orifice, abnormal cushion in the future aortic part of the heart bulb, and
agenesis of the right 4th aortic arch. Could these deviations, which, with
the exception of the missing arcus aortae, were not present after the 7th
day of incubation be the cause of the ventricular septal defect? The
experimentally produced malformation showed that ventricular septal
defects are associated at least to some extent with three of them.
Analysis by means of an injection of a solution of Geigy blue revealed
that the abnormal cushion caused deviation of the coloured blood stream
through the unclosed ventricular septum into the right ventricle and
could, therefore, be considered as a cause of the defect as well. The
observations have demonstrated that a relatively uniform congenital
heart malformation, ventricular septal defect, could have quite different
morphologic pathways of development.
According to a personal communication from Dr. Rychterova (1960)
4 cases of coarctation of the aorta found in human neonates showed a
distinct hypoplasia of the entire left half of the heart, especially of the
left auricle. This demonstrates that the new point of view can be useful
to human pathologists, who are inclined to consider 'left heart' hypoplasia as 'right heart' hypertrophy.
Speaking about 'damage' of the heart loop wall and of the aortic
arches, one must bear in mind that the damage need not necessarily be
of a negative character, but that it can appear as a consequence of local
abundant proliferation (e.g., abnormal bulbar cushion), even though
only temporary.
The teratogenetic critical loci ought not to be analysed merely from
the traditional standpoint of a higher metabolic activity etc., but rather
from the standpoint of their significance in morphogenesis and of their
influence on haemodynamics which conversely act on the morphogenesis of the heart loop and the aortic arches.
It is most probable that a much greater number of embryos are
exposed to 'damage' than would follow from the overall frequency of
cardiovascular malformations: in these embryos the teratogenetic
critical loci were probably not hit and the damage was completely
regulated without leaving manifest alterations. If, however, a teratogenetic critical locus has been hit, then the compensatory, correlative,
and regulative changes would appear controlled by the factors and rules
summarized in the present review.
The solution to the problem of congenital cardiovascular malforma-