Actually, the daily intake of sodium from Paleolithic huntergatherer diet, estimated to be 690 mg, would have been markedly below the lowest estimate of current intake. In modern industrialized society, we are consuming much more salt than biological requirements. Cerebral circulation is vulnerable to excess salt as shown in clinical studies. Experimental studies have also reported detrimental effects of excess salt on cerebral arteries. A high salt diet severely impaired both endotheliumand receptor-mediated vasodilator functions of pial arterioles of rats in the absence of detectable blood pressure changes. In vitro studies showed impaired vascular relaxation mechanisms in isolated rat cerebral arteries. Middle cerebral artery from rats fed a short-term high salt diet exhibited impaired dilation in response to acetylcholine or hypoxia. Excess salt induced oxidative stress, and accelerated spontaneous stroke and bloodbrain barrier disruption in stroke-prone spontaneously hypertensive rats. These experimental studies suggest that pre-existing excess salt impairs cerebral blood flow regulation and BBB integrity, and it may finally aggravate stroke outcome. However, to the best of our knowledge, no study has investigated the relationship between excess salt and the size of subsequent brain infarction produced by middle cerebral artery occlusion. In the present study, we investigated the effects of excess salt on the volume of brain infarction produced by distal MCAO in the rat, and explored the hypothesis that excess salt leads to impaired CBF regulation and/or greater BBB damage in critically ischemic brain tissue. Extravasation of Evans Blue has been used for assessing disruption of BBB after MCAO in animal models owing to its useful property of binding to serum albumin. Albumin and hemoglobin contents determined with surface enhanced laser desorption/ionization-time of flight-mass spectrometry in ischemic brain tissue were increased at 48 h after MCAO in our SHR stroke model. Therefore, in this study, we attempted to directly measure brain albumin and hemoglobin contents as indices of BBB disruption using SELDI-TOF-MS. At 48 h after MCAO, the brain was sampled after transcardial perfusion with 50 mL of saline under deep anesthesia. In the present study, we defined ischemic penumbra as the region that is at risk of being recruited into infarction according to the classic concept of ischemic penumbra.