LAUSR

INTRODUCTION Traumatic shock and hemorrhage (TSH) is a leading cause of preventable death in military and civilian populations. Utilizing a TSH model, we compared Plasma with whole blood (WB) as pre-hospital interventions, evaluating restoration of cerebral tissue oxygen saturation (CrSO2), systemic hemodynamics, colloid osmotic pressure (COP) and arterial lactate, hypothesizing plasma would function in a non-inferior capacity to WB, despite dilution of hemoglobin (Hgb). METHODS Ten anesthetized male rhesus macaques underwent TSH before randomization to receive a bolus of O(-) WB or AB(+) Plasma at T0. At T60, injury repair and shed blood (SB) to maintain mean arterial pressure (MAP) > 65 mmHg began, simulating hospital arrival. Hematologic data and vital signs were analyzed via t-test and two-way repeated measures ANOVA, data presented as mean ± standard deviation, significance = P < 0.05. RESULTS There were no significant group differences for shock time, SB volume or hospital SB. At T0, MAP and CrSO2 significantly declined from baseline, though not between groups, normalizing to baseline by T10. COP declined significantly in each group from baseline at T0 but restored by T30, despite significant differences in Hgb (WB 11.7 ± 1.5 v Plasma 6.2 ± 0.8 g/dL). Peak lactate at T30 was significantly higher than baseline in both groups (WB 6.6 ± 4.9 v Plasma 5.7 ± 1.6 mmol/L) declining equivalently by T60. CONCLUSIONS Plasma restored hemodynamic support and CrSO2, in a capacity not inferior to WB, despite absence of additional Hgb supplementation. This was substantiated via return of physiologic COP levels, restoring oxygen delivery to microcirculation, demonstrating the complexity of restoring oxygenation from TSH beyond simply increasing oxygen carrying capacity.