Acute brain injury followed by hemorrhagic shock (HEM) causes prohibitive mortality in trauma patients because these combined events lead to low cerebral blood flow (CBF) and cerebral oxygen delivery (co2del). Proper treatment therefore requires rapid correction of cerebral perfusion deficits. Previous studies have shown that hypertonic crystalloid resuscitation significantly improves CBF and co2del in a model of brain injury and HEM when compared to lactated Ringer's (LR) solution. The mechanism or mechanisms for this advantage, however, are not well understood. We hypothesized that hypertonic fluid resuscitation would reduce pial arteriolar tone after brain injury and HEM resulting in an increase in CBF when compared to LR resuscitation. We measured cerebral and systemic variables in a porcine model of focal cryogenic brain injury and hemorrhagic shock over a 5-hour period. Swine were randomized to receive either hypertonic sodium lactate (HSL) or LR fluid resuscitation. The HSL resuscitation produced a significant and sustained elevation in cerebral perfusion pressure and pial arteriole diameter (p < 0.05), and a sustained elevation in CBF after brain injury and HEM when compared with LR. These data suggest that hypertonic fluid resuscitation following brain injury and HEM improves CBF, at least in part, by causing vasodilation of cerebral resistance vessels.