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The Mechanisms of cerebral salt wasting syndrome : pathophisiology of hyponatremia following cerebral injury

脑性盐消耗综合征的机制：脑损伤后低钠血症的病理生理学

基本信息

批准号：
18591615
负责人：
MORI Tatsuro
金额：
$ 2.34万
依托单位：
Nihon University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2006
资助国家：
日本
起止时间：
2006 至 2007
项目状态：
已结题

项目摘要

Introduction : Hyponatremia is a common complication in patients with aneurysmal subarachno id hemorrhage (SAH)These patients demonstrate excessive natriuresis, which decreases the total blood volume through osmotic diuresis and increases the risk of symptomatic cerebral vasospasm. It has been demonstrated that the cerebral salt wasting is the cause of hyponatremia following SAH. However, precise mechanisms underlying SAH-induced hyponatremia remain unclear. The purpose of this study is to evaluate whether the rat SAH model exhibits CSW and determine the physiological parameters following SAH. We induced SAH in rats, and the body weight, serum sodium (Na) levels, Na excretion and serum natiretic peptide were measured.Methods : Male Wistar rats were used (n=18). SAH was induced using an endovascular puncture method. The mean arterial blood pressure (MABP), intracranial pressure (ICP), and cerebral blood flow (CBF) were continuously monitored. The urine was cumulatively collected for 12 … More hours post SAH, and the urine Na concentration was determined using a spectrophotometer. The serum Na levels, natriuretic peptide (ANP, BNP) and ADH were measured at 12 hours, and 2 and 4 days following SAH induction.Results : The body weight of SAH rats significantly decreased compared to the sham. The baseline ICP level was 3.5±2.6 mmHg, and was increased to 67.4+17.6 mmHg immediately following the SAH induction. The CBF decreased rapidly and gradually recovered up to 70-80% of the baseline. The urine volume and the total Na excretion significantly increased as comparison to the sham (P<0.05). The serum Na level was significantly decreased at 4 days following SAH (P<0.05). The ANP concentration was significantly decreased in SAH rats (P<0.05), however, the BNP concentration did not change.Conclusions : The present results demonstrate that the SAH-induced endovascular puncture model in rats causes a rapid elevation of ICP and excessive natriuresis. The cause of CSW following SAH was neither ANP nor BNP. Less

导语：低钠血症是动脉瘤性蛛网膜下腔出血（SAH）患者的常见并发症，这些患者表现为过度尿钠，通过渗透性利尿降低总血容量，增加症状性脑血管痉挛的风险。已证实脑盐消耗是SAH后低钠血症的原因。然而，sah诱导的低钠血症的确切机制尚不清楚。本研究的目的是评估大鼠SAH模型是否表现出CSW，并确定SAH后的生理参数。我们诱导SAH大鼠，测定其体重、血清钠（Na）水平、钠排泄量和血清钠肽水平。方法：选用雄性Wistar大鼠18只。采用血管内穿刺法诱导SAH。连续监测平均动脉压（MABP）、颅内压（ICP）和脑血流量（CBF）。累积收集SAH后12小时以上的尿液，用分光光度计测定尿钠浓度。分别于SAH诱导后12小时、2天和4天测定血清钠水平、钠肽（ANP、BNP）和ADH。结果：与假手术相比，SAH大鼠体重明显减轻。基线ICP水平为3.5±2.6 mmHg，在SAH诱导后立即升高至67.4+17.6 mmHg。脑血流迅速下降，并逐渐恢复到基线的70-80%。尿量和总钠排泄量均显著高于对照组（P<0.05）。SAH后4 d血清Na水平显著降低（P<0.05）。SAH大鼠ANP浓度显著降低（P<0.05），而BNP浓度无明显变化。结论：本研究结果表明，sah诱导的大鼠血管内穿刺模型可引起颅内压快速升高和钠尿过多。SAH后CSW的病因既不是ANP也不是BNP。少