Experimental model for investigating hyponatremia after subarachnoid hemorrhage in rats.

Hyponatremia is a common complication in patients with aneurismal subarachnoid hemorrhage (SAH). Such patient demonstrates excessive natriuresis and an increased risk of symptomatic cerebral vasospasm. However, the precise mechanisms underlying SAH induced hyponatremia remain unclear. In the present study, in order to establish an experimental model of hyponatremia following SAH, we induced SAH in rats, and evaluated the serum sodium (Na) levels, Na excretion and physiological parameters. Twenty-four male Wistar rats were used. SAH was induced by an endovascular puncture method. The mean arterial pressure (MAP), intracranial pressure (ICP), and cerebral blood flow (CBF) were monitored continuously. The urine was collected cumulatively for 12 hours after SAH, and the urine Na concentration was determined with a spectrophotometer. The serum Na levels were measured at 12 hrs, 2 and 4 days following the SAH induction. The mean (± standard deviation) baseline ICP was 3.5 ± 2.6 mmHg, and increased to 67.4 ± 17.6 mmHg immediately following induction of SAH. CBF decreased rapidly, and then gradually recovered to 70–80% of baseline. The urine volume and total Na excretion were significantly increased in comparison to those of the sham (P<0.05). The serum Na level was significantly decreased at 4 days following SAH (P<0.05). The present results demonstrated for the first time that rats with SAH exhibited excessive natriuresis. The endovascular puncture model is suitable for investigating hyponatremia that occurs concomitantly with natriuresis and diuresis after SAH.