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Introduction Haemorrhagic shock results in a reduced delivery of oxygen to tissues producing ischemic metabolic insufficiency. Reestablishment of maximal oxygen transport and delivery is the goal of the initial resuscitation. However, aggressive resuscitation strategies could be deleterious by promoting the development of multiple organ failure in relation with mitochondrial dysfunction resulting in impaired cellular oxygen utilization. 1–3 We investigated whether a degraded medical combat causality care (CCC) characterized by prolonged permissive hypotension, no transfusion and normoxia (FiO2=0.21) could prevent or induce mitochondrial dysfunction in kidney compared to hyperoxia (FiO2=1) and blood transfusion.Materials and Methods In a swine model, traumatic-haemorrhagic shock (THS) was obtained by bilateral muscular contusion and femoral fractures associated with 60% withdrawal of the total blood volume (TBV). Shock was prolonged during 90 min (42.2mmHg mean arterial blood pressure at T90) to mimic a combat casualty environment before operating a resuscitation with hypertonic saline for the minimalist medical care (MMC) group (n=6) and with blood for the aggressive medical care (AMC) group (n=6). At T90, AMC group received 20% of their TBV instead of hypertonic saline and FiO 2 was set to 100%. A sham group (n=6, no THS, no fluid resuscitation) served as control. Hemodynamic parameters, lactatemia, renal function and oxygen transport parameters were recorded and analyzed. Oxygen consumption rate of renal tissue was measured by HRR 4hr after the settle of THS to determine respiratory capacities.Results Compared to sham ([creat] 4H=1.15mg/dl), a kidney impairment was induced in both MMC ([creatinine]4H=1.5mg/dl, p=0.006) and AMC groups ([creat]4H=2mg/dl, p=0.049). Interestingly, typical medical CCC care (MMC) preserved respiratory chain complex I (CI)-driven mitochondrial respiration in kidney biopsies while aggressive medical care increases CI-driven mitochondrial respiration compared to MMC and sham groups (p=0.006 and p=0.049, respectively).Conclusions We showed that aggressive oxygen delivery therapy could lead to an increase in mitochondrial respiration that could be a biomarker of renal bioenergetic dysfunction as previously shown. The results of this study ultimately suggest that preservation of mitochondrial function should be given greater consideration in resuscitation strategies.Abstract A08 Figure 1Respiratory chain complex I (CI)-driven mitochondrial respiration in kidney biopsies (OXPHOS CI). Mitochondrial respiration is expressed as oxygen flux (pmol/mg wet tissue/s)References Asfar P, Singer M, Radermacher P. Understanding the benefits and harms of oxygen therapy. Intensive Care Med. 2015 Jun;41(6):1118–21.Collard CD, Gelman S. Pathophysiology, Clinical Manifestations, and prevention of ischemia-reperfusion injury. Anesthesiology. 2001 Jun 1;94(6):1133.Go KL, Lee S, Zendejas I, Behrns KE, Kim JS. Mitochondrial dysfunction and autophagy in hepatic ischemia/reperfusion injury. BioMed Research International. 2015;2015:1–14.Disclosure The authors declare no competing interests.