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[围生期缺氧性脑病的发病机制]

[Pathogenesis of hypoxic encephalopathy during pre- and peri-natal periods].

作者信息

Shimada M

机构信息

Department of Pediatrics, Shiga University of Medical Science, Ohtsu.

出版信息

No To Hattatsu. 1994 Mar;26(2):111-2.

PMID:8136181
Abstract

Hypoxic encephalopathy during the late gestation and perinatal period occupies a large part as a cause of mentally and physically handicaps. An extensive study on the pathogenesis and pathophysiology of the hypoxic brain damage is, therefore, the matter of urgency to minimize the occurrence of handicapped children. The main factors and/or processes relating to hypoxic or hypoxic-ischemic brain damage are (1) structural and functional immaturity of the brain vascular system and (2) a metabolic cascade triggered by hypoxia. As the following metabolic cascade subsequent to hypoxia has been partly made clear; (a) disturbance of the energy metabolism, (b) excessive release of excitatory amino acids and subsequent activation of NMDA and K/Q receptors at the cell membrane, (c) collapse of the membrane ion pump, and (d) increase in turnover of membrane phospholipids.

摘要

妊娠晚期和围产期的缺氧性脑病是导致智力和身体残疾的主要原因之一。因此,广泛研究缺氧性脑损伤的发病机制和病理生理学,对于尽量减少残疾儿童的发生至关重要。与缺氧或缺氧缺血性脑损伤相关的主要因素和/或过程包括:(1)脑血管系统的结构和功能不成熟;(2)缺氧引发的代谢级联反应。由于缺氧后的以下代谢级联反应已部分明确:(a)能量代谢紊乱;(b)兴奋性氨基酸过度释放,随后细胞膜上的NMDA和K/Q受体激活;(c)膜离子泵功能崩溃;(d)膜磷脂周转率增加。

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