Oxidative Stress and Inflammation during Simulated Hemorrhage

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2018-05

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Park, Flora S.

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Background: Hemorrhage is a leading cause of potentially preventable death in both civilian and military trauma settings. Lower body negative pressure (LBNP) is a validated, non-invasive, and reproducible approach to simulate hemorrhage by inducing central hypovolemia in healthy conscious humans. The oxidative stress and inflammatory response to simulated hemorrhage via LBNP has not been quantified. We hypothesized that systemic markers of oxidative stress and inflammation will increase with application of maximal LBNP. Methods: 15 human subjects (11M/4F) were recruited for a LBNP exposure to presyncope (chamber pressure was progressively reduced every 5-min in a stepwise manner). Arterial pressure and stroke volume (SV) were measured continuously via finger photoplethysmography, muscle oxygen saturation (SmO2) was measured via near-infrared spectroscopy, and venous blood samples were collected. Plasma samples were analyzed for a global marker of oxidative stress [F2-isoprostanes (F2-IsoP)] and inflammatory markers (IL-1beta, IL-2, IL-4, IL-6, IL-10, TNF-alpha, and CRP). Results: The magnitude of central hypovolemia, indexed by % change SV, ranged from -27-74%. Maximal LBNP induced a -12.6?2.6% decrease in mean arterial pressure (MAP, P[less than]0.001). F2-IsoP increased by 28.5?11.6% (P=0.05) from baseline (24?2 pg/ml) to presyncope (29?3 pg/ml). The increase in F2-IsoP was not associated with % change SV (r=0.21, p=0.46), % change MAP (r=0.05, p=0.86), the maximum level of LBNP attained (r=0.35, p=0.20), or % change SmO2 (r=0.05, p=0.90). TNF-alpha and CRP increased by 3.7% (p=0.02, n=4) and 26.9% (p=0.07, n=6). TNF-alpha and CRP responses were not associated with % change SV (r=0.50, p=0.50 and r=0.36, p=0.49), % change MAP (r=0.91, p=0.09 and r=0.006, p = 0.99), the maximum level of LBNP attained (r=0.39, p=0.61 and r=0.23, p=0.66), or % change SmO2 (r=0.75, p=0.46 and r=0.90, p=0.11). Conclusion: Simulated hemorrhage induced by LBNP to presyncope elicited an increase in oxidative stress and inflammation. These findings have important implications for the study of hemorrhage using LBNP, and future investigations of targeted interventions.

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