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蛛网膜下腔出血大鼠的脑性盐耗综合征:模型、机制及工具

Cerebral salt wasting in subarachnoid hemorrhage rats: model, mechanism, and tool.

作者信息

Kojima Jun, Katayama Yoichi, Moro Nobuhiro, Kawai Hiroyuki, Yoneko Maki, Mori Tatsuro

机构信息

Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan.

出版信息

Life Sci. 2005 Apr 1;76(20):2361-70. doi: 10.1016/j.lfs.2004.11.010.

DOI:10.1016/j.lfs.2004.11.010
PMID:15748629
Abstract

Cerebral salt wasting (CSW) frequently occurs concomitantly with aneurysmal subarachnoid hemorrhage (SAH). CSW induces excessive natriuresis and osmotic diuresis, and reduces total blood volume. As a result, the risk of symptomatic cerebral vasospasm may be elevated. Therefore, it is important to determine the mechanism of CSW. The purpose of this study was to evaluate whether the rat SAH model exhibits CSW and to investigate the relationship between CSW and natriuretic peptides. A SAH model was produced in 24 rats by perforating a cerebral artery with a nylon thread up through the common carotid artery. To evaluate CSW, urine was cumulatively collected from SAH onset to 12 hours and sodium (Na) excretion was analyzed. Body weight and hematocrit were analyzed before and after SAH onset. Concentrations of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in plasma were also analyzed. Urine volume and total Na excretion of SAH rats were significantly higher than those of sham rats (p<0.05). Body weight of SAH rats significantly decreased and hematocrit significantly increased (p < 0.05). ANP concentration was significantly decreased in SAH rats (p<0.05). However, BNP concentrations did not change. This study demonstrated for the first time that a rat SAH model exhibited CSW. It was suggested that the cause of CSW was neither ANP nor BNP. In addition, this rat SAH model will be useful for study of CSW after SAH.

摘要

脑性盐耗综合征(CSW)常与动脉瘤性蛛网膜下腔出血(SAH)同时发生。CSW会引发过度利钠和渗透性利尿,并减少总血容量。结果,有症状的脑血管痉挛风险可能会升高。因此,确定CSW的机制很重要。本研究的目的是评估大鼠SAH模型是否表现出CSW,并研究CSW与利钠肽之间的关系。通过用尼龙线经颈总动脉向上穿刺脑动脉,在24只大鼠中建立SAH模型。为评估CSW,从SAH发作开始至12小时累积收集尿液,并分析钠(Na)排泄情况。在SAH发作前后分析体重和血细胞比容。还分析了血浆中心房利钠肽(ANP)和脑利钠肽(BNP)的浓度。SAH大鼠的尿量和总钠排泄量显著高于假手术大鼠(p<0.05)。SAH大鼠的体重显著下降,血细胞比容显著升高(p<0.05)。SAH大鼠的ANP浓度显著降低(p<0.05)。然而,BNP浓度没有变化。本研究首次证明大鼠SAH模型表现出CSW。提示CSW的原因既不是ANP也不是BNP。此外,该大鼠SAH模型将有助于研究SAH后的CSW。

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Life Sci. 2005 Apr 1;76(20):2361-70. doi: 10.1016/j.lfs.2004.11.010.
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