2007 Fiscal Year Final Research Report Summary
The Mechanisms of cerebral salt wasting syndrome : pathophisiology of hyponatremia following cerebral injury
| Project/Area Number |
18591615
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Nihon University |
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Principal Investigator |
MORI Tatsuro Nihon University, School of Dentistry at MATSUDO, Lecturer (00318437)
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| Co-Investigator(Kenkyū-buntansha) |
KATAYMA Yoichi Nihon University, School of Medicine, Professor (00125048)
KAWAMATA Tatsuro Nihon University, School of Medicine, Associate Professor (20234122)
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| Project Period (FY) |
2006 – 2007
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| Keywords | Subarachnoid hemorrhage / Cerebral casospasm / hvoontremia / cerebral salt wasting / itotal blood volume / intracranial pressure |
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| Research Abstract |
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
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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
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