HYPEROXIA PRODUCES NEURONAL NECROSIS IN THE RAT
HYPEROXIA PRODUCES NEURONAL NECROSIS IN THE RAT
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DOI：
10.1097/00005072-198605000-00006
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发表时间：
1986-05-01
影响因子：
3.2
通讯作者：
LIN, MR
中科院分区：
文献类型：
--
作者：
AHDABBARMADA, M;MOOSSY, J;LIN, MR
新生Sprague-Dawley大鼠在正常大气压下接受3小时纯氧（100%O2）治疗后发生广泛的脑神经元坏死。神经元坏死（NN）是最严重的新生儿期和不显着与先进的成熟。在10、15和20日龄的大鼠和在正常大气压下呼吸纯氧3小时的成年大鼠中，其形态特征是最小的和不同的。在新生大鼠中，高氧血症的NN在形态学和细胞病理学上与缺氧诱导的相同动物不同。高血氧NN类似于人类早产儿中描述的发作性高血氧症的NN。核破裂的神经元损伤在海马下托、丘脑、脑干网状核和小脑颗粒细胞中最为突出。超微结构研究表明，核和细胞质膜损伤的神经元和电子致密脂滴的细胞积累。在人类早产新生儿中由高氧产生的NN的发病机制可能与细胞膜的脂质过氧化有关，例如在其他实验和体外研究中由氧自由基诱导的脂质过氧化，当抗氧化细胞防御（主要是酶，如超氧化物歧化酶）被淹没时。
Widespread cerebral neuronal necrosis occurred in newborn Sprague-Dawley rats submitted to three hours of pure oxygen (100% O2) at normal atmospheric pressure. Neuronal necrosis (NN) was most severe in the immediate newborn period and less marked with advanced maturation. It was minimal and different in its morphological characteristics in rats 10, 15 and 20 days old, and in adults breathing pure oxygen at normal atmospheric pressure for three hours. In the newborn rat, hyperoxemic NN was different in topography and cytopathology from that induced by hypoxia in the same animals. Hyperoxemic NN was similar to the NN described in human premature infants submitted to episodic hyperoxemia. Neuronal damage with karyorrhexis was most prominent in the subiculum of the hippocampus, thalamus, reticular nuclei of the brain stem and the granular cells of the cerebellum. Ultrastructural studies demonstrated nuclear and cytoplasmic membrane damage in neurons and the cellular accumulation of electron-dense lipid droplets. The pathogenesis of NN produced by hyperoxia in the human permature newborn infant may be related to lipid peroxidation of cell membranes such as that induced by oxygen-free radicals in other experimental and in vitro studies, when the anti-oxidant cellular defenses (mainly enzymes such as superoxide dismutase) are overwhelmed.