Browsing by Subject "LBNP"
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Item Oxidative Stress and Inflammation during Simulated Hemorrhage(2018-05) Park, Flora S.; Rickards, Caroline A.; Mallet, Robert T.; Goulopoulou, Styliani; Warren, Joseph E.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.Item Sympathetic Cardiac Influence and Arterial Blood Pressure Instability(2002-09-01) Formes, Kevin John; Shi, Xiangrong; Downey, H. Fred; Gwirtz, Patricia A.Formes, Kevin John, Sympathetic Cardiac Influence and Arterial Blood Pressure Instability. Master of Science (Biomedical Sciences) September 2002, 51 pp., 3 tables, 5 illustrations, 36 references. This study was designed to determine the role of β1-adrenoreceptors in arterial blood pressure (ABP) regulation during an orthostatic challenge. Metoprolol was used to block β1-adrenoreceptors. Atropine, a peripheral and central acting muscarinic blocker, was used to inhibit vagal influences on heart rate. Lower body negative pressure (LBNP) was used to stimulate an orthostatic hypotensive stimulus before and after receptor blockade. Metoprolol administration significantly increased baroreflex sensitivity (BRS) and significantly decreased the reflex increase baroreflex sensitivity (BRS) and significantly decreased the reflex increase in plasma renin activity (PRA) in response to a hypotensive stimulus. Therefore we suggest that the attenuation of PRA is counterbalanced by an increased heart rate reserve, which allows the heart rate to increase more in response to decreases in venous return. This increase in cardiac responsiveness was abolished with the administration of atropine. Therefore, we conclude that acute administration of metoprolol causes (i) improved ABP stability, as indicated by a diminished augmentation of low frequency (LF) ABP variability and (ii) attenuates the increase in PRA during LBNP induced central hypovolemic challenge.Item THE ROLE OF DIFFERENTIAL OXYGEN DISTRIBUTION BETWEEN THE BRAIN AND PERIPHERAL TISSUES ON TOLERANCE TO INDUCED CENTRAL HYPOVOLEMIA(2013-04-12) Kay, VictoriaPurpose: Maintenance of cerebral perfusion and oxygenation is essential for survival from hemorrhage. As individuals vary in tolerance to reduced blood volume (e.g., central hypovolemia), we hypothesized that subjects with high tolerance (HT) will maintain cerebral oxygenation compared to low tolerant (LT) subjects, which will be associated with greater peripheral vasoconstriction. Methods: 13 human subjects were instrumented for cerebral (ScO2) and muscle (SmO2) oxygenation (near-infrared spectroscopy, NIRS), then completed a step-wise presyncopal-limited lower body negative pressure (LBNP) protocol. Total hemoglobin (HbT) was calculated as an index of local peripheral resistance (inverse relationship) at the muscle. Results: Progressive decreases in ScO2 were observed in LT subjects (n=5) from -45 mmHg LBNP (P≤0.01 compared to baseline), while Sc02 did not change throughout LBNP for the HT subjects (n=8; P≥0.44). Sm02 decreased at -30 and -60 mmHg LBNP (P≤0.01) in the HT group with concomitant increases in resistance (decreases in HbT; P≤0.03). In contrast, both Sm02 (P=0.01) and HbT (P=0.06) only decreased at -60 mmHg LBNP in the LT group. Conclusions: In support of our hypothesis, increased tolerance to progressive central hypovolemia was associated with maintained cerebral oxygenation, due, in part, to earlier onset of peripheral vasoconstriction.