OBJECTIVE: Myelomeningocele is a neural tube defect resulting in an exposed spinal cord, which leads to irreversible neurologic damage at birth. We proposed 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 laparotomy to expose the gravid uterus; a hysterotomy exposed the fetal hindlimbs and back. A three to four level lumbar laminectomy was performed, and the dura over the posterior spinal cord was removed. At 30 days of gestation, the does underwent C-section for fetal harvest, and total fetal number, length, 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 confirmed a spina bifida-like lesion of their spinal cords. CONCLUSIONS: We successfully created an exposed spinal cord defect in the fetal rabbit model similar to the lesion found in humans. Advantageous because of low animal cost, relatively large fetal size, multiple fetuses per pregnancy, and short total gestation, this model will allow us to study the mechanism of injury to the exposed spinal cord, and perhaps develop strategies to repair human myelomeningoceles. Copyright 2000 S. Karger AG, Basel.
OBJECTIVE: Myelomeningocele is a neural tube defect resulting in an exposed spinal cord, which leads to irreversible neurologic damage at birth. We proposed 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 laparotomy to expose the gravid uterus; a hysterotomy exposed the fetal hindlimbs and back. A three to four level lumbar laminectomy was performed, and the dura over the posterior spinal cord was removed. At 30 days of gestation, the does underwent C-section for fetal harvest, and total fetal number, length, 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 confirmed a spina bifida-like lesion of their spinal cords. CONCLUSIONS: We successfully created an exposed spinal cord defect in the fetal rabbit model similar to the lesion found in humans. Advantageous because of low animal cost, relatively large fetal size, multiple fetuses per pregnancy, and short total gestation, this model will allow us to study the mechanism of injury to the exposed spinal cord, and perhaps develop strategies to repair human myelomeningoceles. Copyright 2000 S. Karger AG, Basel.
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