Hemorrhage is one of the main causes responsible for the impairment of blood flow, with subsequent tissue hypoperfusion and hypoxia. As the circulating blood volume decreases, oxygen consumption (VO 2 ) remains constant for a considerable amount of blood loss. When the oxygen delivery (DO 2 ) drops below a critical level, i.e. 10 mL O 2 / min per kg, VO 2 falls abruptly. This signifies a blood volume loss of approximately 50%, associated with substantial reduction in cardiac output and mixed venous oxygen saturation [1]. At this stage of ischemia, deep tissue hypoxia leads the severely O 2 -deprived cell to prime for generation of ROS, upon O 2 re-entry during reperfusion [2]. Cellular priming consists of ATP depletion, since ATP degrades, reaching the level of hypoxanthine with concurrent xanthine oxidase accumulation. This situation is associated with either absolute O 2 restriction (no-flow state) or prolonged O 2 debt (low flow state) [3]. The profuse and sudden oxygen re-entry at resuscitation acts as a cofactor, allowing xanthine oxidase to convert hypoxanthine to uric acid. The resulting by-products are superoxide anions (O 2 -) and hydrogen peroxide (H 2 O 2 ), representing the main molecules of the initial oxidative burst [2]. The aforementioned reactive oxygen species, along with the free radicals generated by NADPH oxidase within the neutrophils, attack peroxidating cell membranes. Consequently, ischemia/ reperfusion injury occurs, the global equivalent of which is hemorrhagic shock and resuscitation.Recently, the importance of limited resuscitation [4-7] has been widely acknowledged. Patients with penetrating truncal trauma, in which resuscitation was delayed, had a higher survival rate to discharge (70%) compared with promptly resuscitated patients (62%, P = 0.04) [4]. Likewise, a systemic review of animal studies [5] has also shown a lower risk of death in animals resuscitated to hypotensive levels than in animals resuscitated to normotensive levels (P \ 0.00001). The small volume resuscitation with fluids such as hypertonic saline [6] or albumin 25% [7] has similarly shown a higher survival rate compared with infusion of isotonic fluids.The approach of attempting to lessen reperfusion injury by adjusting the inspired O 2 may apply either before [8] or during [9-12] resuscitation. As far as the first case is concerned, the impact of inspired oxygen concentration on tissue oxygenation (tPO 2 ) in the absence of resuscitation was the subject of a study from Dyson et al. [8], published in this issue of the journal. The latter case is represented by hypoxemic resuscitation [9][10][11][12]; a process in which hypoxemia is applied during the first few minutes of resuscitation and, as shock reverses, it gradually turns to normoxemia.In the aforementioned study [8], tissue oxygenation improves at mild (less than 20%) blood volume losses similarly to normovolemia, in response to higher inspired oxygen admixtures. Adversely, at significant (more than 50%) blood volume losses, higher inspired oxygen admixture...