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To determine the effects of primary blast injury (PBI) on survival and the physiological response to resuscitation after hemorrhagic shock.Air-blast injury is a significant clinical problem that can reduce blood oxygenation and modify the response to hemorrhage. PBI has specific physiological effects that have not been fully accounted for in resuscitation strategies. Permissive hypotension is a widely adopted strategy in trauma resuscitation. However, the choice of resuscitation strategy requires a full understanding of the mechanisms of injury and their physiological consequences.Terminally anesthetized pigs were divided into 4 groups and subjected to either air-blast injury (B) or no blast (S). All received a controlled hemorrhage of 30% blood volume and resuscitation with 0.9% saline to a normotensive (Normot, systolic blood pressure 110 mm Hg) or hypotensive (Hypot, 80 mm Hg) end point for up to 8 hours. (n = 6 in each B and n = 8 in each S subgroup).Survival time was significantly shorter with Hypot (P < 0.0001 Peto log rank). The effect was in the animals subjected to B (P = 0.0005) (mean survival time [95% CI]; BNormot 422 [313–531] vs. BHypot137 [94–181] min), but not those given S (P = 0.06) (SNormot 480 [all survived] vs. SHypot 352 [210–494] min). PBI exacerbated a profound metabolic acidosis during Hypot, possibly due to an overwhelming compromise in tissue oxygen delivery.Prolonged hypotensive resuscitation is not compatible with survival after primary blast. Casualties most likely to be in this category are those injured by blast in confined spaces or by enhanced blast weapons. The risk of rebleeding associated with normotensive resuscitation needs to be balanced with the metabolic derangement associated with hypotensive resuscitation.