Browsing by Subject "lower body negative pressure"
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Item Cardiac Autonomic Response to Hypovolemia --- Effect of Age(1997-08-01) Wang, Hong-Wei; Raven, Peter B.; Shi, Xiangrong; Caffrey, James L.Objective: The beat-to-beat variation in heart rate reflects the dynamic response of the cardiovascular control systems to physiological perturbations such as respiration and postural change. The heart rate variation (HRV) is a part of the rapidly reacting component of cardiovascular homeostasis largely influenced by parasympathetic and sympathetic input. Thus, beat-to-beat variation in heart rate can be used as a measure of cardiac autonomic responses. The standard deviation of R-R interval is a measure of the overall variability in heart rate and has been shown to decrease with aging (9,23). This measure, however, can not identify individual sources of the variation. Spectral analysis reduces a signal to its constituent frequency components and the relative power of these components has been indicated related to parasympathetic mediation, combined sympathetic and parasympathetic mediation, and sympathetic mediation (1, 14, 17). Limited data are available regarding power spectral analysis of heart rate variation to study aging changes under orthostatic stress. An attenuated cardiac sympathetic nerve activity was found in older group vs younger individuals (7, 11, 19) during posture change. However, these studies were carried out using either posture change from to upright or passive head-up tilt. During these posture changes, both cardiopulmonary baroreceptors (i.e., intrathoracic hypovolemia) and arterial baroreceptors (postural hypotension) were unloaded. Therefore, it is unclear whether there is any difference in the HR variability between the young and the elderly during unloading of cardiopulmonary baroreceptors (or low-pressure baroreceptors) alone. In this study, we investigated the age difference in cardiac autonomic modulation of heart rate during unloading of cardiopulmonary baroreceptors with or without systemic arterial hypotension. For the purpose, we examined beat-to-beat heart rate variability in both the time and frequency domain using power spectral analyses in healthy individuals from ages 18 to 68 under basal conditions and in response to graded lower body negative pressure induced central hypovolemia. Not only individual low and high frequency spectral content were analyzed and those parameters were compared in order to find a quantitative evaluation of sympathetic and parasympathetic modulation and under the graded lower body negative pressure.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 Peripheral and Central Muscarinic Cholinergic Receptors in Arterial Blood Pressure Regulation(1999-12-01) Wray, David Walter; Shi, Xiangrong; Gwirtz, Patricia A.; Raven, Peter B.Wray, David Walter, Peripheral and Central Muscarinic Cholinergic Receptors in Arterial Blood Pressure Regulation. Master of Science (Biomedical Sciences), December, 1999, 70 pp., 7 tables, 8 illustrations, references, 83 titles. This study was designed to test the hypothesis that an age-related vagal dysfunction compromises arterial blood pressure (ABP) regulation. Changes in heart rate (HR) and ABP during lower body negative pressure (LBNP) were compared between ten elderly (≥60 yrs) and ten young (≤30 yrs) adults. A separate, young group (n=10) was also assessed following muscarinic cholinergic (MC) blockade with atropine (central and peripheral receptor blockade) or glycopyrrolate (peripheral receptor blockade) to simulate vagal dysfunction. During the onset of LBNP -40 too, orthostatic hypotension (OH) was observed in both the older subjects and the post-blockade younger subjects, with a diminished HR response. Furthermore, the reflex response to hypertensive stimuli was augmented in the post-blockade younger subjects, also associated with a diminution in HR response. We concluded that age-related or pharmacologically stimulated vagal dysfunction compromises ABP regulation during hypotensive and hypertensive stimuli, and that the difference between atropine and glycopyrrolate was insignificant.Item Sex Differences in Oxidative Stress and Inflammation Responses During and After Simulated Hemorrhage(2020-05) Barnes, Haley J.; Rickards, Caroline A.; Hodge, Lisa M.; Mallet, Robert T.; Goulopoulou, StylianiHemorrhage (i.e., massive blood loss) induces an oxidative stress and inflammatory response that can persist even following hemostasis and resuscitation. Premenopausal females exhibit a survival advantage following hemorrhage compared to young males. In this study, we hypothesized that young males would elicit a greater oxidative stress and inflammatory response compared to young females, both during and after a simulated hemorrhage via lower body negative pressure (LBNP). Young, healthy human subjects (10F; 10M) participated in a stepwise-LBNP protocol to presyncope. Venous blood samples were collected at baseline, presyncope, and 1-h into recovery (i.e., following "resuscitation"). The oxidative stress response was assessed via circulating F2-isoprostanes (F2-IsoP) using gas chromatography-negative ion chemical ionization-mass spectrometry. The inflammatory response was assessed via circulating tissue necrosis factor-α (TNF-α), C-Reactive Protein (CRP), thymus and activation-regulated chemokine (TARC), and interleukin (IL)-5, IL-6, IL-7, and IL-10, using a MSD® Multiplex assay. LBNP tolerance time was similar between male and female subjects (Males, 1592±124 s vs. Females, 1437 ± 113 s; P = 0.37). There was no effect of time or sex on the absolute or relative change in F2-IsoP during or after LBNP (P ≥ 0.12). However, male subjects exhibited a greater pro-and anti-inflammatory response during and after LBNP compared to female subjects (Notable markers at 1-h recovery compared to baseline, IL-6: Males, 101.4 ± 138.9% vs. Females, 12.3 ± 34.0%, P = 0.06; IL-10: Males, 71.1 ± 133.3% vs. Females, -2.2 ± 11.8%; P = 0.06). These data suggest that there may be a potential sex difference in the inflammatory response to simulated hemorrhage.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 Cerebral Oxygenation and Perfusion on Tolerance to Central Hypovolemia(2016-12-01) Kay, Victoria L.; Caroline A. Rickards; Robert T. Mallet; Michael L. SmithTolerance to central hypovolemia, including hemorrhage, is highly variable between individuals. The role of cerebral oxygenation and regional cerebral perfusion on tolerance to central hypovolemia has not been explored. Protection of posterior cerebral perfusion may be an important factor in tolerance, as the posterior circulation supplies blood to the autonomic and respiratory control centers in the brain stem. Additionally, despite the reduction in cerebral oxygen delivery with central hypovolemia via decreased flow, the role of compensatory increases in oxygen extraction and subsequent cerebral tissue oxygenation on tolerance have not been identified. The oscillatory pattern of cerebral blood flow has recently been identified as a contributing factor to improving tolerance to central hypovolemia, and may be more important than the protection of absolute flow. This finding was demonstrated when comparing high vs. low tolerant individuals, and in subjects who exhibited increased tolerance to central hypovolemia while breathing against inspiratory resistance. We hypothesized that healthy human subjects with naturally high tolerance to central hypovolemia, and subjects breathing against inspiratory resistance under hypovolemic stress would exhibit 1) protection of cerebral oxygen saturation (ScO2); 2) prolonged preservation of cerebral blood flow in the posterior versus anterior cerebral circulation, and; 3) higher LF oscillations in cerebral blood flow. The major findings from these investigations are: 1) subjects with high tolerance to central hypovolemia exhibited protection of ScO2 and velocity in the posterior cerebral circulation; 2) LF oscillations did not play a role in the protection of ScO2; 3) resistance breathing improved tolerance to central hypovolemia, but not via protection of ScO2 or velocity in either the anterior or posterior cerebral circulation, and; 4) resistance breathing was associated with increased high frequency oscillatory power in arterial pressure, anterior and posterior cerebral blood velocity, and ScO2. We conclude that individuals with naturally high tolerance to central hypovolemia exhibit protection of cerebral tissue oxygenation and prolonged preservation of perfusion within the posterior cerebral circulation, but not in the anterior circulation, thus delaying the onset of presyncope. Improved tolerance to central hypovolemia via resistance breathing was not related to these mechanisms, but may have been associated with increased depth of breathing, subsequently decreasing intracranial pressure and increasing cerebral perfusion pressure.