Amniocentesis dysmelia in rats.

Amniocentesis performed on Day 15½ of gestation caused dysmelia in 85 of 143 offspring of Sprague-Dawley and Wistar strain rats. Almost all defects were of reduction type, only 3 hind limb postaxial supernumerary digits being seen. Defect intensity graded from longitudinal splitting of the phalanges, through phalangeal suppression, to very severe growth retardation of the long limb bones and the limb girdle. The lesions in the 2 strains were indistinguishable from each other. Subcutaneous haemorrhages were frequently present and could take the form of blebs. Hind limbs were more frequently and, on average, more severely affected than fore limbs. Left-sided defects were more severe than right-sided ones. Sections of tibiae from defects of intermediate severity showed impaired endosteal, periosteal and endochondral osteogenesis. The total limb defects may be regarded as a combination of (a) retarded growth in long bones, (b) arrested or aberrant differentiation of the bones in the digital rays and (c) destruction of digital structures by haemorrhage and possibly localized ischaemic tissue necrosis. Among the associated defects were cleft palate, anomalies of the abdominal wall, genitourinary tract defects and short umbilical cord. Some aspects of the possible part played by the chorion and amnion in limb defect production have been reviewed and the tentative conclusion reached that the foetal membranes do not significantly compress the foetus.