Influence of age on the cerebral lesions in an immature rat model of cerebral hypoxia-ischemia: A light microscopic study
Influence of age on the cerebral lesions in an immature rat model of cerebral hypoxia-ischemia: A light microscopic study
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DOI：
10.1016/s0165-3806(97)00036-9
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发表时间：
1997-06-18
期刊：
影响因子：
--
通讯作者：
Vannucci, SJ
中科院分区：
文献类型：
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作者：
Towfighi, J;Mauger, D;Vannucci, SJ
最常用的新生儿脑缺氧-缺血模型由7天出生后大鼠模型与颈总动脉结扎和低氧血症相结合组成。神经病理学研究表明，该7天出生后大鼠模型与类似的成人模型在整体脑易损性、损伤类型和分布方面存在重大差异。目前尚不清楚在动物的发育过程中，大脑脆弱性的这些变化是如何以及何时发生的。为了确定这一点，我们研究了出生后2至30天的大鼠组。动物接受单侧颈总动脉结扎，然后在8%氧气中呼吸30、60、90或120 min，并在24或72 h恢复期检查其大脑。由于2-3日龄大鼠脑缺氧缺血性损伤的抗性，用5%O-2代替8%O-2。结果表明：（i）在出生后2至7天，颈总动脉结扎侧的脑损伤的严重程度总体上增加。随着年龄的增长，发育中的动物大脑病变的频率也会增加。(ii)海马在出生后2-3天对缺氧缺血性损伤具有显著的抵抗力，但逐渐变得脆弱，到出生后13天，海马的脆弱性远远超过皮质。(iii)皮质病变的变化，主要是柱状细胞死亡层状选择性神经元死亡，在13岁出生后。(iv)在发育过程中，海马各区的相对脆弱性也发生了显着变化。在出生后的前5天，海马区域的相对脆弱性是相似的，但随着动物的发育和海马脆弱性的增加，病变往往涉及特定的区域，而不涉及其他区域。出生后13天，CA 1和外侧CA 3发展增加的脆弱性，而内侧CA 3和筋膜齿变得相对抵抗和出生后21天，成人模式的CA 1选择性脆弱性接近。这些变化的潜在机制，在区域的脆弱性，脑缺氧缺血在发展过程中，应寻求复杂的区域解剖，功能和代谢的变化，发生大脑成熟。
The most frequently used model of neonatal cerebral hypoxia-ischemia consists of a 7-day postnatal rat model with combined common carotid artery ligation and hypoxemia, Neuropathologic studies have shown major differences between this 7-day postnatal rat model and a similar adult model in regard to overall cerebral vulnerability, type and distribution of lesions. It is not clear how and when during animals' development these changes in cerebral vulnerability take place. To determine this we studied groups of rats of 2 to 30 postnatal days. The animals underwent unilateral common carotid artery Ligation followed by breathing in 8% oxygen for 30, 60, 90, or 120 min and their brains were examined at 24- or 72-h recovery intervals. Due to resistance Of 2-3-day-old rats to develop cerebral hypoxic-ischemic damage, 5% O-2 was used instead of 8% O-2. The results indicate that: (i) There is an overall increase in severity of cerebral lesions on the side of common carotid artery ligation between 2 and 7 postnatal days. There is also an increase in the frequency of cerebral lesions in developing animals with increasing age. (ii) Hippocampus is remarkably resistant to hypoxic-ischemic insult at 2-3 postnatal days but becomes progressively vulnerable, and by age 13 postnatal days hippocampal vulnerability far exceeds that of cortex. (iii) Cortical lesions change from predominantly columnar cell death to laminar selective neuronal death at age 13 postnatal days. (iv) Also significant changes occur in relative vulnerability of various hippocampal regions during development. During the first 5 postnatal days relative vulnerability of hippocampal regions is similar, but as the animals' development proceeds and hippocampal vulnerability increases lesions tend to involve specific regions while sparing others. By age 13 postnatal days CA1 and lateral CA3 develop increased vulnerability while medial CA3 and fascia dentata become relatively resistant and by 21 postnatal days adult pattern of CA1 selective vulnerability is approached. The underlying mechanisms for these changes in regional vulnerability to cerebral hypoxia-ischemia during development should be sought in complex regional anatomic, functional, and metabolic alterations that take place as brain matures.