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Introduction Haemorrhagic shock results from in a reduced delivery of oxygen to tissues thus producing ischemic metabolic insufficiency. It has been previously shown that Adenosine-Lidocaine-Magnesium therapy (ALM) upregulated key genes of mitochondrial oxidative phosphorylation, thus powering mitochondrial function. 1 2 We used high resolution respirometry (HRR) to determine mitochondrial respiratory capacity specific to respiratory chain complexes and investigated if infusion of an ALM solution prevented mitochondrial dysfunction in a porcine combat relevant model of traumatic-haemorrhagic shock (THS)Materials and Methods THS was obtained by bilateral muscular contusion and femoral fractures associated with 60% withdrawal of the total blood volume (TBV). ALM was slowly infused at T60 min and shock was prolonged during 90 min (42.2 mmHg [35.8–53] mean arterial blood pressure, n=6) to mimic a combat casualty (CC) environment before operating a resuscitation with 10% of their TBV at T90 with FiO 2=1 and 10% more at T180 min. Control group (n=6) underwent the same procedure, but no ALM infusion. A sham group (n=6) underwent the same procedure without THS and fluid resuscitation. Haemodynamic parameters, lactatemia, renal function and oxygen transport parameters were recorded and analysed. Oxygen consumption rate of renal tissue was measured by HRR 4 hr after the settle of THS to determine respiratory capacities: OXPHOS respiratory chain complex I (CI)Results ALM infusion had a protective effect on arterial lactate level at T90 (5.67±0.76 mmol/l with ALM vs. 7.99±0.91mmol/l without ALM, p=0.039) and after the transfusion (5.49±0.87 mmol/l vs. 7.92±0.95 mmol/l, p=0.046) ( figure 1). ALM seemed to limit arterial pH drop (7.41±0.02 with ALM vs. 7.35±0.01 without ALM, p=0.057). Renal maximal oxidative phosphorylation through CI (OXPHOS CI) was significantly increased in the traumatic-haemorrhagic shock group compared to the sham group (27.77±2.71 vs. 18.32±0.91 pmol/s.mg, p<0.006) and ALM therapy failed to modify this OXPHOS CI over-activity (26,55 ± 2,09 in ALM group).Conclusions ALM treatment does not seem to confer mitochondrial respiratory support despite a beneficial effect observed in blood lactate and arterial pH. Nonetheless, by mitigating lactic acidosis, ALM therapy remains a promising approach for haemorrhagic shock resuscitation in austere environments, especially since adenosine, lidocaine and magnesium are all potential candidates for lyophilization to allow easy use and long-term storage for these drugs.Abstract P03 Figure 1Arterial lactate levels during the experimental procedureReferences Letson HL, Morris JL, Biros E, Dobson GP. Adenosine, lidocaine, and Mg2+ fluid therapy leads to 72-hour survival after hemorrhagic shock: a model for studying differential gene expression and extending biological time. Journal of Trauma and Acute Care Surgery. 2019 Sep;87(3):606–13.Letson HL, Granfeldt A, Jensen TH, Mattson TH, Dobson GP. Adenosine, lidocaine, and magnesium support a high flow, hypotensive, vasodilatory state with improved oxygen delivery and cerebral protection in a pig model of noncompressible hemorrhage. Journal of Surgical Research. 2020 Sep;253:127–38.Disclosure The authors declare no competing interests