Oxidative Stress During Simulated Hemorrhage Elicited by Lower Body Negative Pressure




Kay, Victoria
Park, Flora
Anderson, Garen
Sprick, Justin
Rickards, Caroline


Journal Title

Journal ISSN

Volume Title



Purpose: Hemorrhage is a leading cause of potentially preventable death in both civilian and military trauma settings. Hemorrhage also elicits an oxidative stress response as a direct result of losing blood volume, or as an indirect response to ischemia-reperfusion injury. Lower body negative pressure (LBNP) is a well validated, non-invasive, and reproducible approach to simulate hemorrhage by inducing central hypovolemia in healthy conscious humans. The oxidative stress response to simulated hemorrhage via LBNP has not been quantified. We hypothesized that systemic markers of oxidative stress would increase with application of LBNP. Methods: 15 healthy human subjects (11M, 4F; 27 ± 1 y) were recruited for a step-wise LBNP exposure to presyncope (systolic blood pressuresymptoms). After baseline, LBNP pressure progressively decreased every 5 minutes to -15, -30, -45, -60, -70, -80, -90, and -100 mmHg. Arterial pressure and stroke volume were measured continuously via finger photoplethysmography, and venous blood samples were collected at baseline and during the LBNP profile. Plasma samples were analyzed for F2-isoprostanes, a global marker of oxidative stress, via gas chromatography/mass spectrometry. Results: The magnitude of central hypovolemia, indexed by the % change in stroke volume, ranged from a 27% to 74%. LBNP induced a -12.6 ± 2.6 % decrease in MAP (%Δ MAP) from baseline (P Conclusion: Simulated hemorrhage elicited by step-wise LBNP to presyncope elicited an increase in a global marker of oxidative stress. These findings have important implications in the study of hemorrhage and potential application of targeted interventions. Funding Source: US Army Medical Research and Materiel Command (W81XWH-11-2-0137) & Owens Foundation Grant. Analysis of eicosanoids (F2-isoprostanes) were performed in the Vanderbilt University Eicosanoid Core Laboratory.