新生大鼠缺氧性脑损伤模型的建立及评价

Establishment and evaluation of a rat model of neonatal hypoxic brain injury

目的模拟新生儿出生窒息,建立新生大鼠缺氧性脑损伤模型。方法将新生大鼠短暂置于100%氮气环境中,建立出生窒息的模型。18只新生大鼠随机分为对照组、缺氧10 min组、缺氧20 min组,采用神经行为学观察、Nissl染色及透射电镜观察脑组织病理变化等方法,评价动物模型的可靠性。结果缺氧过程新生大鼠均出现全身紫绀、意识障碍等精神行为的异常。Nissl染色可见缺氧10 min海马CA1区部分神经元肿胀,缺氧20 min神经元损伤加重。尼氏染色阳性细胞数量缺氧10 min组低于对照组(P<0.05),缺氧20 min组显著低于对照组(P<0.01)。超微结构显示:缺氧10 min神经元出现染色质边集,微血管内皮细胞空泡变性;缺氧20 min神经元坏死,核溶解,细胞器模糊不清。微血管周围星胶细胞脚板、细胞突起均肿胀。结论新生大鼠短暂置于100%氮气中,可建立简便可靠的新生鼠缺氧性脑损伤模型。

Objective To establish a rat model mimicking the brain injury caused by neonatal hypoxia. Methods Neonatal rats were transiently exposed to 100% nitrogen gas. Eighteen rats were randomly divided into normal control group,10 min hypoxia group and 20 min hypoxia group. The reliability of the model was evaluated by behavior analysis and pathological examination of the brain tissues by means of Nissl staining and transmission electron microscopy. Results Transient hypoxia in neonatal rats resulted in systemic cyanosis,abnormal mental behavior and conscious disturbance. Nissl staining showed that hypoxia for 10 min led to the swelling of the partial neurons in the hippocampal CA1 region and that hypoxia for 20 min caused the neuron injury more severe. Compared with normal control group,the number of Nissl staining positive cells was decreased in 10 min hypoxia group（ P〈0. 05） and 20 min hypoxia group（ P〈0. 01）. Ultrastructure of the neurons revealed the margination of chromatin and the vacuolar degeneration of microvascular endothelial cells during 10 min of hypoxia. Also the neuron necrosis was observed in 20 min hypoxia group,featured by dissolved nuclei,indistinct organelles,and the swelling of both baseboard and processes of astrocytes. Conclusion A simple and reliable animal model of hypoxic brain injury is successfully established by transient exposure of neonatal rats to 100% nitrogen gas.