Pravastatin has neuroprotective effects against aging but its role in brain injury remains unclear. This study evaluated the effects of pravastatin on the ultrastructural changes and hemorheological parameters in rats after traumatic brain injury (TBI) of right parietal cortical contusion by a controlled weight-dropping method. There were three groups: (I) Sham operated group; (II) TBI + vehicle (saline) group; and (III) TBI + pravastatin group. Right parietal craniectomy was performed in all groups. In TBI + pravastatin group, pravastatin was administered orally at a dose of 1 mg/kg every day for 7 days starting at 24 hours after the injury. Plasma viscosity, erythrocyte deformability and erythrocyte aggregation were measured from blood samples of all rats on 2nd, 7th and 15th days. At the same time electron microscopic study was done on designated days for groups II and III. Treatment with pravastatin markedly increased aggregation amplitude and gamma Isc max values and significantly decreased erythrocyte deformability but did not change plasma viscosity in 2 weeks time. Ultrastructural parameters such as perinuclear edema, mitochondrial swelling and intraneuronal vacuoles were detected in lower degree in the statin group when compared to the saline group, especially decreased demyelinization and endothelial detachment was prominent. As a result, the hyperviscosity state with increased erythrocyte aggregation and decreased erythrocyte deformability induced by pravastatin in this study was accompanied by an improvement of the ultrastructural findings in TBI. This hyperviscosity state may be a compensatory mechanism to increase the oxygenation of the injured tissue by inducing the release of antiaggregant and vasodilatory substances by increasing shear stress. Therefore, we suggest that prolonged pravastatin usage may exert affirmative effects on traumatic brain injury conditions by increasing blood viscosity.