The "stright-jacket" syndrome in chicks. II. Mechanism of development

In a longitudinal study including measurement of the pressure in the amniotic cavity, amniotomy, and planimetric evaluation of the size of the amniotic sac, we investigated the development of the "strait jacket" syndrome in White Leghorn chicken embryos injected intraamniotically (ia) or paraamniotically on the fourth day of incubation with histone or embryotoxic serum, with the following results. Hyperlordosis and eventration developed as an outcome of tonic contraction of the amnion, which was observed only three hours after ia administration. Contraction of the amnion caused elevation of the intraamniotic pressure, which, 12 hours after ia injection, attained a mean value of 22.4 Pa (2.3 mm H2O). This value was not only significantly higher than the mean for control embryos (3.9 Pa), but it was critically close to the mean fluid pressure in the brain vesicles. Loss of the latter overpressure caused the vesicles to collapse, and the walls shriveled and exencephaly developed. Paraamniotic injection was not followed by either contraction of the amnion, or significant increase in intraamniotic pressure. This did not prevent heart malformations and cranioschisis of various extent. The majority of cardiovascular malformations were probably the hemodynamic consequence of overfilling of the intraembryonic vascular bed, which was one of the early signs of the effect question. Cranial-vault defects can be causally associated with the formation of amnionic adhesion and fusion with the epidermal ectoderm. This observation stresses the significance of the embryonic membranes and the fluid pressures within them for the development of certain congenital deformities and concentrates attention on teratological study of substances that induce protracted contraction of smooth muscle.