Limited role of inducible nitric oxide synthase in blood-brain barrier function after experimental subarachnoid hemorrhage.

Excessive nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) may play a pivotal role in blood-brain barrier (BBB) breakdown following subarachnoid hemorrhage (SAH). We investigated if the inhibition of iNOS could reduce BBB breakdown and cerebral edema, thereby leading to improved outcome 24 h after SAH. Forty male rats were assigned to three groups: control, SAH, and treatment groups. SAH was induced by perforating the bifurcation of the internal carotid artery. The neurological score and the mortality were evaluated 24 h after the surgery. The expression of iNOS, the concentration of NO metabolites, morphological changes in neuronal cells, water content, and IgG leakage were also evaluated. The expression of iNOS, as well as the concentration of NO metabolites, was elevated after SAH. Treatment with p-Toluenesulfonate decreased both the expression of iNOS and the concentration of NO metabolites. However, there was no significant change in water content, BBB disruption, or morphological findings between the SAH group and the treatment group. Furthermore no significant differences in neurological score or mortality were observed. The iNOS inhibitor failed to reduce BBB breakdown, brain edema, and neuronal cell death and failed to improve the neurological score and the mortality 24 h after SAH.