摘要
目的 探讨宫内窒息后的新生鼠脑病理变化 ,并与生后的状况相联系。 方法 制备宫内不同程度缺血缺氧 (15、30、45及 6 0 m in)及再灌注 (缺血缺氧 15 m in后再灌注 1、4、8、15及 2 4h)模型 ,观察剖宫产后新生鼠的一般状况并进行光、电镜下的脑病理观察。 结果 轻度的宫内缺血缺氧可引起神经元的变性 ,但生后的一般状态无明显改变 ;严重的宫内缺血缺氧当时即可引起胎死宫内 ,此时神经元表现为坏死。宫内轻度窒息的新生鼠 ,出生时一般状态尚可 ,但再灌注后状态越来越差 ,与神经元再灌注后呈现的进行性凋亡过程相平行。 结论 急性宫内缺血缺氧可以引起胎死宫内 ,神经元表现为坏死 ,在坏死之前再灌注将引起凋亡 ;再灌注后进行性凋亡过程是某些宫内窒息新生儿在出生后状态越来越差的主要原因 ,新生儿缺氧缺血性脑病的病理变化可能在宫内已经开始发生。
Objective To study the relationship between the pathology changes in brain of rat infant with intrauterine asphyxia and the situations of the rats after birth. Methods 9 rats with gestational age of 21 days served as control group, 24 as ischemia hypoxia group and 30 as reperfusion group. Intrauterine ischemia hypoxia was produced by clamping the uterine blood supplying for 15,30,45 and 60 mins respectively. Other rats were reperfused for 1,4,8,15 and 24 hours after clamping for 15 minutes. All of them would be delivered by cesarean section at time points and the situations of newborns were observed. Meanwhile, the pathologic changes of cerebral tissues were observed by light and electronic microscope. Results Mild intrauterine ischemia and hypoxia could lead to the degeneration of neurons, but the situations of newborn seemed normal. While the severe ischemia would cause the intrauterine fetal death immediately, and the cerebral tissues showed necrosis. Those newborn rats of reperfusion group seemed well, but developed badly after being reperfused, which were parallel to the developing apoptosis of cerebral neurons. Conclusions Intrauterine ischemia and hypoxia can cause fetal death with the cerebral cell necrosis. Reperfusion will lead to apoptosis of the neuron,which is the main cause of that newborns seemed well after birth while worsened gradually. The pathologic changes of newborn HIE might already happen before birth.
出处
《中华围产医学杂志》
CAS
2002年第4期294-296,I002,共4页
Chinese Journal of Perinatal Medicine
