Inhibition of nitric oxide synthase partially attenuates alterations in the blood-cerebrospinal fluid barrier during experimental meningitis in the rat.

The permeability of the blood-cerebrospinal fluid (blood-CSF) barrier is increased upon exposure to lipopolysaccharides during bacterial meningitis. Lipopolysaccharides induce nitric oxide (NO) synthase in a variety of cells. Increased meningeal NO production and blood-CSF barrier permeability were observed in a rat model of meningitis. Administration of aminoguanidine, an inhibitor of NO synthase, blocked meningeal NO production and significantly attenuated permeability changes in the blood-CSF barrier. It is hypothesized that pathological production of NO may contribute to the disruption of the blood-CSF barrier during meningitis.