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[失血性休克时脑缺血损伤的分子与细胞机制]

[Molecular and cellular mechanisms of ischemic damage of the brain in hemorrhagic shock].

作者信息

Kozhura V L, Solov'eva Zh V, Novoderzhkina I S, Nosova N V

出版信息

Anesteziol Reanimatol. 1994 May-Jun(3):24-8.

PMID:8080122
Abstract

General lightening of caryoplasma, the appearance of destructive areas in which electron-optic density was undetectable, ruptures in chromatin chains, changes in the nature of structural organization of euchromatic areas at the expense of density redistribution have been found in the nuclei of brain cortex oligodendrogliocytes and astrocytes by electron microscopy of caryoplasma of the nuclei from light neurons during experiments on anesthetized adult mongrel dogs weighing 9 to 26 kg recovered after a 4-hour hemorrhagic shock (BP 40 mm Hg). The nuclei of dark neurons and oligodendrogliocytes had matrix structure similar to control. The nuclei of astrocytes had marked matrix lightening with the formation of large zones in which electron-optic density was undetectable. It is evident that the degree of chromatin destruction in different neurons was not identical in hemorrhagic shock and depended on the functional neuronal activity. It has been established that there is a significant increase in the activity of nuclear Ca2+, Mg(2+)-depended endonucleases associated with chromatin and irreversibly cleaving ds- and ss-chromatin DNA chains. We believe that an increase in Ca2+, Mg(2+)-depended DNA-endonuclease activity should be considered an important pathogenetic factor in destructive processes that take place in the nuclei of brain cortex neurons in severe hemorrhagic shock.

摘要

在对体重9至26千克、经4小时失血性休克(血压40毫米汞柱)后恢复的成年杂种麻醉犬进行实验时,通过对轻神经元细胞核的核质进行电子显微镜观察,发现大脑皮质少突胶质细胞和星形胶质细胞核内出现核质普遍变淡、出现电子光学密度不可测的破坏区域、染色质链断裂以及常染色质区域结构组织性质改变(以密度重新分布为代价)。暗神经元和少突胶质细胞的细胞核具有与对照相似的基质结构。星形胶质细胞的细胞核有明显的基质变淡现象,并形成了电子光学密度不可测的大区域。显然,在失血性休克中,不同神经元中染色质的破坏程度并不相同,且取决于神经元的功能活性。已经确定,与染色质相关且不可逆地切割双链和单链染色质DNA链的核Ca2+、Mg(2+)依赖性内切核酸酶的活性显著增加。我们认为,Ca2+、Mg(2+)依赖性DNA内切核酸酶活性的增加应被视为严重失血性休克时大脑皮质神经元细胞核中发生的破坏过程的一个重要致病因素。

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