关于缺血性脑水肿发病机制的一个新概念：自由基和类花生酸的相关性。

A novel concept on the pathogenetic mechanism underlying ischaemic brain oedema: relevance of free radicals and eicosanoids.

作者信息

Asano T, Shigeno T, Johshita H, Usui M, Hanamura T

机构信息

Department of Neurosurgery, Saitama Medical Centre, Saitama Medical School, Tokyo, Japan.

出版信息

Acta Neurochir Suppl (Wien). 1987;41:85-96. doi: 10.1007/978-3-7091-8945-0_11.

DOI:10.1007/978-3-7091-8945-0_11

PMID:2833076

Abstract

A survey on literature reports and our own experimental studies on the pathogenetic mechanisms underlying ischaemic brain oedema is given and a new concept proposed. In regional incomplete ischaemia the lipoxygenase activity is enhanced, presumably caused by an increase of free radicals and hydroperoxides, leading to an enhancement of endothelial Na+, K+-AtPase and increased sodium and water transport from blood to brain. The aggravation of brain oedema and post-ischaemic hypoperfusion following recirculation appears to be mainly due to an activation of the cyclo-oxygenase pathway with release of oxidants from PGG2, which causes non-specific but detrimental damage to the endothelial and parenchymal cells. This new concept may open future perspectives in treatment which are briefly discussed.

摘要

本文对缺血性脑水肿发病机制的文献报道及我们自己的实验研究进行了综述，并提出了一个新的概念。在局部不完全缺血中，脂氧合酶活性增强，推测是由自由基和氢过氧化物增加所致，导致内皮细胞钠钾ATP酶活性增强，钠和水从血液到脑的转运增加。再灌注后脑水肿加重和缺血后灌注不足似乎主要是由于环氧化酶途径的激活以及PGG2释放出氧化剂，这会对内皮细胞和实质细胞造成非特异性但有害的损伤。这个新概念可能为治疗带来新的前景，本文对此进行了简要讨论。