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

简介：低钠血症是蛛网膜下腔出血（SAH）患者的常见并发症。这些患者表现出过度钠尿，通过渗透性利尿减少总血容量，并增加症状性脑血管痉挛的风险。研究表明，脑盐耗是SAH后低钠血症的原因。然而，蛛网膜下腔出血诱导低钠血症的确切机制尚不清楚。本研究的目的是评价大鼠SAH模型是否表现出CSW，并确定SAH后的生理参数。方法：雄性Wistar大鼠（n=18），采用SAH模型，测定大鼠体重、血钠（Na）水平、Na排泄量及血清利钠肽（Na+）水平。使用血管内穿刺方法诱导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 ...更多信息 在SAH后24小时，使用分光光度计测定尿Na浓度。分别于造模后12 h、2 d、4 d测定血清钠、利钠肽（ANP、BNP）和抗利尿激素（ADH）水平。基线ICP水平为3.5±2.6 mmHg，在SAH诱导后立即增加至67.4 ± 17.6 mmHg。CBF迅速下降并逐渐恢复至基线的70-80%。与假手术组相比，尿量和总钠排泄量显著增加（P<0.05）。SAH后4d血清钠水平明显降低（P<0.05）。结论：蛛网膜下腔出血（SAH）大鼠血管内穿刺模型可引起颅内压（ICP）迅速升高和尿钠排泄增加。蛛网膜下腔出血后CSW的病因既不是ANP也不是BNP。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