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[新生兔室管膜下层缺氧变化的超微结构研究]

[An ultrastructural investigation of changes in hypoxia in the subependymal layer of the newborn rabbit].

作者信息

Koshino T, Tsuyuki Y, Yokota A, Tsunoda Y, Araki T, Asano G

机构信息

Department of Obstetrics and Gynecology, Nippon Medical School, Tokyo, Japan.

出版信息

Nihon Ika Daigaku Zasshi. 1990 Feb;57(1):55-63. doi: 10.1272/jnms1923.57.55.

DOI:10.1272/jnms1923.57.55
PMID:2329181
Abstract

Fetal and neonatal hypoxia is suggested as a noticeable risk factor related to the occurrence of subependymal hemorrhages. To investigate the cause of newborn subependymal hemorrhages, a 0 day old newborn rabbit was exposed to either 5 or 10 minutes hypoxia by N2 box. After exposure, the brain was observed by optical and electric microscope using horseradish peroxidase (HRP) as the protein tracer to study the change in the capillary permeability. The result obtained were as follows: 1) In the newborn rabbit blood gas analysis, PO2 (mmHg) decreased more in the 5 and 10 min hypoxia groups than the control group which used the N2 box. pH and BE changes were similar to PO2 (mmHg). On the other hand, PCO2 (mmHg) increased proportionately. These results indicated that this hypoxic method changed blood gas and caused acidosis. 2) In the optical microscopic examination, the 0 day old newborn rabbit brain was found to have a thin subependymal layer. We could not find obvious subependymal hemorrhage using optical microscope. 3) In the electric microscopic examination, HRP was found in the cavity of the brain capillary at the subependymal layer and was slightly incorporated into the pinocytic vesicle of the lumen on the control. Since the tight junction filled the roll out, HRP was not found outside the capillary. 4) The 5 min hypoxia group caused astrocyte foot swelling, edema and slight opening of the tight opening of the tight junction. HRP was passed through the tight junction, but not outside the capillary. 5) The 10 min hypoxia group caused destruction of astrocyte and edema around the capillary. The tight junction was more opened than in the 5 min hypoxia group and HRP leaked out of the capillary through the tight junction. From the findings mentioned above, it is suggested that our hypoxic model increased permeability of the capillary in subependymal layers and that this change might be the first ultrastructural change before the onset of subependymal hemorrhages.

摘要

胎儿和新生儿缺氧被认为是与室管膜下出血发生相关的一个显著风险因素。为了研究新生儿室管膜下出血的原因,一只出生0天的新生兔通过氮气箱暴露于5分钟或10分钟的缺氧环境中。暴露后,使用辣根过氧化物酶(HRP)作为蛋白质示踪剂,通过光学显微镜和电子显微镜观察大脑,以研究毛细血管通透性的变化。得到的结果如下:1)在新生兔血气分析中,5分钟和10分钟缺氧组的PO2(mmHg)下降幅度比使用氮气箱的对照组更大。pH和BE的变化与PO2(mmHg)相似。另一方面,PCO2(mmHg)成比例增加。这些结果表明这种缺氧方法改变了血气并导致酸中毒。2)在光学显微镜检查中,发现出生0天的新生兔大脑室管膜下层很薄。使用光学显微镜我们未发现明显的室管膜下出血。3)在电子显微镜检查中,在室管膜下层的脑毛细血管腔内发现了HRP,在对照组中它被轻微地纳入管腔的吞饮小泡中。由于紧密连接充满了间隙,在毛细血管外未发现HRP。4)5分钟缺氧组导致星形胶质细胞足肿胀、水肿以及紧密连接的紧密开口轻微张开。HRP穿过了紧密连接,但未穿出毛细血管。5)10分钟缺氧组导致星形胶质细胞破坏和毛细血管周围水肿。紧密连接比5分钟缺氧组张开得更大,HRP通过紧密连接从毛细血管中漏出。从上述发现可以看出,我们的缺氧模型增加了室管膜下层毛细血管的通透性,并且这种变化可能是室管膜下出血发生前的首个超微结构变化。

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