Intracranial hypertension (ICH) is a common and serious complication of bacterial meningitis (M). The mechanism of ICH is incompletely delineated but probably includes contributions from brain edema, increased CSF volume and increased cerebral blood volume (CBV). We have previously documented the contribution of CBV to ICH in experimental M (EM) and have recently demonstrated by near-infrared spectroscopy (NIRS) that there is an increase in cerebral deoxygenated hemoglobin (Hb) in EM, suggesting vasodilation or stasis in the cerebral venous vascular bed (Ped Res 1996 40:759-63). The purpose of the present study was to investigate the role of nitric oxide (NO) as a candidate mediator of these abnormalities. M was induced in New Zealand white rabbits by intracisternal injection of ≈106 S.pneumoniae, type 3. Relative concentrations of cerebral total Hb(THb) and deoxygenated Hb (DHb) (expressed as variation in density units [v/d u]) were measured by NIRS and intracranial pressure (mm Hg) was measured by transducer at 18 h of infection. Three groups of animals were studied: uninfected controls (U), infected (I), and I given L-NAME (I + L-NAME), a NO synthase inhibitor (25 mg/kg). Results are shown below as mean ± SD(#). Table

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I rabbits had increased ICP, THb and DHb compared to U, which was blocked by treatment with L-NAME. A possible mechanism by which this could occur would be through an increase in CBV as indicated by increased THb, and more specifically, by an increase in blood in the cerebral venous vascular bed, as suggested by increased DHb. Supported in part by PHS Grant P20 NS 32553.