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颅内出血时局部脑缺血的发病机制:钾的因果影响?

On the pathogenesis of regional cerebral ischemia in intracranial hemorrhage: a causal influence of potassium?

作者信息

Edvinsson L, Lou H C, Tvede K

出版信息

Pediatr Res. 1986 May;20(5):478-80. doi: 10.1203/00006450-198605000-00019.

Abstract

Cerebral ischemia and intracranial hemorrhage are the most important causes of perinatal brain damage and their pathogenesis seems to be interrelated. Several components in blood have been shown to cause contraction of cerebral blood vessels. In the present study we examined the changes with time of the concentration of standard electrolytes in a mixture of blood and mock cerebrospinal fluid, whether these changes may affect cerebrovascular tone, and if calcium blockers could influence such an effect. Extracellular K+ increased to about 23 mM 4 days after mixing when half of the mixture consisted of blood, and remained nearly constant for at least 8 days thereafter. Using isometric recording of circular tension in a controlled tissue bath it was found that isolated human pial arterioles, small arteries, and feline middle cerebral arteries contracted markedly when K+ exceeded 10 and 20 mM, respectively. It is concluded that neonatal perihemorrhagic ischemia may be, at least partly, due to leakage of K+ from the erythrocytes. The contractile effect of extracellular K+ is effectively counteracted by Ca++ entry blockers, which therefore may have a role in the prevention of perihemorrhagic ischemia in neonates.

摘要

脑缺血和颅内出血是围产期脑损伤的最重要原因,其发病机制似乎相互关联。血液中的几种成分已被证明可引起脑血管收缩。在本研究中,我们检测了血液与模拟脑脊液混合后标准电解质浓度随时间的变化,这些变化是否会影响脑血管张力,以及钙阻滞剂是否会影响这种效应。当混合物的一半为血液时,混合4天后细胞外钾离子浓度增加到约23 mM,此后至少8天保持几乎恒定。使用等长记录法在可控组织浴中记录环形张力,发现当钾离子分别超过10 mM和20 mM时,分离的人软脑膜小动脉、小动脉和猫大脑中动脉会明显收缩。得出的结论是,新生儿围出血性缺血可能至少部分是由于钾离子从红细胞中泄漏所致。细胞外钾离子的收缩作用可被钙离子内流阻滞剂有效抵消,因此钙离子内流阻滞剂可能在预防新生儿围出血性缺血中发挥作用。

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