Objective: Myelomeningocele is a neural tube defect resulting in an exposed
spinal cord, which leads to irreversible neurologic damage at birth. We pr
oposed development of a fetal rabbit model of myelomeningocele to study in
utero spinal cord injury and repair strategies. Methods: New Zealand white
rabbits (n = 10) at 22 days of gestation (term = 31 days) underwent laparot
omy to expose the gravid uterus; a hysterotomy exposed the fetal hindlimbs
and back. A three to four level lumbar laminectomy was performed, and the d
ura over the posterior spinal cord was removed. At 30 days of gestation, th
e does underwent C-section for fetal harvest, and total fetal number, lengt
h, weight, and the presence or absence of a spinal defect were recorded for
all viable fetuses. Results: All injured fetuses were smaller and weighed
less than the nonoperated littermate controls, and histologic examination c
onfirmed a spina bifida-like lesion of their spina I cords. Conclusions: We
successfully created an exposed spinal cord defect in the fetal rabbit mod
el similar to the lesion found in humans. Advantageous because of low anima
l cost, relatively large fetal size, multiple fetuses per pregnancy, and sh
ort total gestation, this model will allow us to study the mechanism of inj
ury to the exposed spinal cord, and perhaps develop strategies to repair hu
man myelomeningoceles. Copyright (C) 2000 S. Karger AG, Basel.