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使用钙通道阻滞剂治疗蛛网膜下腔出血所致的血管痉挛。

Treatment of vasospasm due to subarachnoid hemorrhage with calcium entry blockers.

作者信息

Przuntek H, von Baumgarten F, Mertens H G

出版信息

Eur Neurol. 1986;25 Suppl 1:86-92. doi: 10.1159/000116103.

DOI:10.1159/000116103
PMID:3530777
Abstract

Cerebral vasospasm is the most important factor causing neurological deterioration later than 72 h after subarachnoid hemorrhage (SAH). The few clinical studies investigating the effect of calcium entry blockers on SAH demonstrate that patients treated with nimodipine have a better clinical outcome. The experimental data do not explain the mechanism of the observed clinical effect. Nimodipine does not reverse large vessel spasm, but it seems that it dilates microvessels and that it exerts a protective effect on nervous tissue by influencing metabolic processes not yet known.

摘要

脑血管痉挛是蛛网膜下腔出血(SAH)后72小时后导致神经功能恶化的最重要因素。少数研究钙通道阻滞剂对SAH影响的临床研究表明,接受尼莫地平治疗的患者临床结局更好。实验数据并未解释所观察到的临床效果的机制。尼莫地平不能逆转大血管痉挛,但它似乎能扩张微血管,并通过影响尚不清楚的代谢过程对神经组织发挥保护作用。

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Eur Neurol. 1986;25 Suppl 1:86-92. doi: 10.1159/000116103.
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