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

前言：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，这些患者表现出过多的钠尿，通过渗透性利尿减少总血量，增加症状性脑血管痉挛的风险。已有研究表明，SAH后低钠血症的原因是脑部盐耗。然而，SAH诱导的低钠血症的确切机制仍不清楚。本研究旨在评价大鼠蛛网膜下腔出血(SAH)模型是否存在CSW，并测定SAH后的生理参数。建立大鼠蛛网膜下腔出血模型，测定体重、血钠、钠排泄量和血清内分泌多肽。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)。累积收集尿液12…SAH后数小时，用分光光度计测尿钠浓度。分别于SAH诱导后12h、2d、4d测定大鼠血钠、心钠素(ANP、BNP)和ADH水平。结果：SAH大鼠体重明显低于假手术组。基础值为3.5±2.6 mm Hg，SAH诱导后即刻升至67.4±17.6 mm Hg。脑血流量迅速下降，并逐渐恢复至基线的70-80%。与假手术组比较，模型组大鼠尿量和尿钠排泄量显著增加(P&lt；0.05)。SAH后第4天血钠水平显著下降(P&lt；0.05)。SAH大鼠血浆ANP浓度显著降低(P&lt；0.05)，而BNP浓度无明显变化。结论：SAH大鼠血管内穿刺术后，颅内压迅速升高，钠尿量增加。SAH后CSW的原因既不是ANP也不是BNP。较少

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