Central nervous system malformations induced by triamcinolone acetonide in nonhuman primates: pathogenesis.
Central nervous system malformations induced by triamcinolone acetonide in nonhuman primates: pathogenesis.
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非人灵长类动物中曲安奈德诱发的中枢神经系统畸形：发病机制。
DOI：
10.1002/tera.1420380310
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Hendrickx,AG
中科院分区：
文献类型：
--
作者：
Tarara,RP;Wheeldon,EB;Hendrickx,AG
TAC诱发的脑膨出的发病顺序与神经管关闭后中脑突出，随后的生长发育导致大脑和小脑突出的假说是一致的。该模型可用于阐明脑膨出的发病机制，并促进将该缺陷与其他闭合不全状态进行比较的进一步研究。用醋酸曲安奈德(TAC)对16只妊娠恒河猴(Macaca Mulatta)进行肌肉注射(10 mg/kg)，连续5天，从妊娠第23天开始。在GD35、42、50或70行子宫切开术摘除胚胎，并进行大体和组织学检查。用图像分析仪测量顶盖和导水管的长度、面积、周长和周长。处理标本的变化提示顶盖内部或腹侧的力量导致背部突出、吻部-后部拉伸和衰减。还测量了头、桥和颈曲的角度。治疗标本的头曲角度越尖锐，颈曲角度越轻，可能代表着继发于间充质缺乏症的方向改变。然而，在处理的标本中，脑桥弯曲的角度不那么尖锐，这表明神经管的内在变化。这表明脑膨出可能是间充质和神经管异常的综合结果。
The pathogenetic sequence for TAC‐induced encephalocele is in agreement with hypotheses proposing that neural tube closure is followed by protrusion of the mesencephalon, with subsequent growth and development resulting in herniation of the cerebrum and cerebellum. This model could serve to clarify the pathogenesis of encephalocele and to stimulate further study in comparing this defect to other dysraphic states. Triamcinolone acetonide (TAC) was administered intramuscularly (10 mg/kg) to 16 pregnant rhesus monkeys (Macaca mulatta) for 5 alternate days of pregnancy, beginning on gestational day (GD) 23. Conceptuses were removed by hysterotomy at GD 35, 42, 50, or 70 and examined grossly and histologically. Length, area, and perimeter of the tectum and aqueduct area and perimeter were measured with an image analyzer. Changes in treated specimens were suggestive of forces within or ventral to the tectum resulting in dorsal protrusion, rostral‐posterior stretching, and attenuation. The angle of the cephalic, pontine, and cervical flexures was also measured. The more acute angle of the cephalic flexure and less acute cervical flexure of treated specimens could represent altered orientation secondary to a mesenchymal deficiency. However, the less acute angle of the pontine flexure in treated specimens suggests an intrinsic alteration in the neural tube. This suggests that encephalocele may result from a combination of mesenchymal and neural tube abnormalities.