THE IMPACT OF POSTTRAUMATIC STRESS DISORDER ON PERIPHERAL VASCULAR FUNCTION

The physiological manifestations of posttraumatic stress disorder (PTSD) have been associated with an increase in risk of cardiovascular disease (CVD) independent of negative lifestyle factors. Peripheral vascular dysfunction may be a mechanism by which PTSD increases CVD risk via increases in oxidative stress, inflammation, and/or sympathetic nervous system activity. PURPOSE: This study sought to examine peripheral vascular function in those with PTSD compared to age-matched controls. METHODS: Eight individuals with PTSD (5 women, 3 men; age 22 ± 2 years), and sixteen healthy controls (CON; 10 women, 6 men, 23 ± 2 years), participated in the study. Leg vascular function was assessed via passive leg movement (PLM) technique and evaluated with Doppler ultrasonography. PLM-induced increases in leg blood flow were quantified as peak change in blood flow from baseline (ΔPeak LBF) and blood flow area under the curve (LBF AUC). RESULTS: Significant differences in leg vascular function were revealed between groups. The PTSD group reported significantly lower ΔPeak LBF (PTSD: 294.16 ± 54.16; CON: 594.78 ± 73.70 ml∙min-1; p = 0.01) and LBF AUC (PTSD: 57.23 ± 24.37; CON: 169.92 ± 29.84 ml; p = 0.02) when compared to the CON group. CONCLUSION: This study revealed that lower limb vascular function is impaired in individuals with PTSD when compared to healthy counterparts.https://scholarscompass.vcu.edu/gradposters/1043/thumbnail.jp

Determining the Impact of Increased Physical Activity on Improving Sleep Quality in Young Adults

Determining the Impact of Increased Physical Activity on Improving Sleep Quality in Young Adults Disturbed sleep, defined as any alteration to normal sleep patterns, has been linked to poor cardiovascular health and an increase in cardiovascular disease (CVD) risk. These negative sleep patterns are highly prevalent with 35% to 41% of individuals in the United States reported some form of disturbed sleep. Although high amounts of physical activity (PA) are often associated with high sleep quality, little is known about PA’s effectiveness to improve different aspects of sleep (e.g. duration vs quality) and the mechanisms to which it can improve sleep quality. Purpose: The study sought to determine the ability of increased PA to improve sleep efficiency in healthy young adults. Methods: Nineteen young adults (25±4 yrs) were recruited for this study. Subjects wore an accelerometer (Actigraph GT3x-BT) for a total of three weeks to record daily physical activity (step count; low, moderate, and vigorous physical activity) and sleep variables (efficiency, wake after sleep onset, number of nightly awakenings, time per awakening, and total sleep time). Subjects maintained normal physical activity levels for the first week (BL), then increased their step count by an average of 5,000 steps/day across the next two weeks (W1 and W2). Heart rate variability (HRV) and venous blood draws were collected weekly to assess sympathetic activity and inflammation, respectively. Results: The physical activity intervention resulted in significant increases (p \u3c 0.001) in step-count for both W1 (13163 ± 3184) and W2 (12168 ± 3619) when compared to BL (8648 ± 2615 steps/day). No significant differences from BL were observed when examining sleep efficiency (BL: 83.8 ± 6.4; W1: 85.5 ± 4.0; W2: 84.2 ± 6.1 %), sympathetic-vagal balance, and inflammatory marker concentrations in W1 and W2. A significant correlation was revealed when assessing the change in sleep efficiency from BL to W1 (r = 0.81, p \u3c 0.001) and BL to W2 (r = 0.52, p = 0.02) when compared to initial sleep efficiency values. Conclusion: This study revealed that although young healthy individuals appear to lack improvements in sleep efficiency with an increase in physical activity, those who reported the lowest sleep quality had the greatest improvements in sleep efficiency following an increase in physical activity. Therefore, the findings of the study suggest that although increasing physical activity can improve sleep quality, a potential “ceiling effect” may occur, as when sleep quality is adequate, augmenting physical activity no longer has a substantial effect.https://scholarscompass.vcu.edu/gradposters/1058/thumbnail.jp

Vascular Dysfunction and Posttraumatic Stress Disorder: Examining the Role of Oxidative Stress and Sympathetic Activity

Purpose: The physiological manifestations of posttraumatic stress disorder (PTSD) have been associated with an increase in risk of cardiovascular disease (CVD) independent of negative lifestyle factors. The goal of the study was to better elucidate the mechanisms behind the increased CVD risk by examining peripheral vascular function, a precursor to CVD. Moreover, this study sought to determine the role of oxidative stress and sympathetic nervous system (SNS) activity in PTSD-induced vascular dysfunction. Methods: Sixteen individuals with PTSD (10 women, 6 men; age 24 ± 4 years), and twenty-four healthy controls (CTRL; 15 women, 9 men, 24 ± 4 years), participated in the study. The PTSD group participated in two visits, consuming either a placebo or antioxidant cocktail (AO - vitamins C and E and alpha lipoic acid) prior to their visits, in a randomized order. Arm vascular function was assessed via the reactive hyperemia- induced flow mediated dilation of the brachial artery (BAFMD) technique and evaluated with Doppler ultrasonography. Brachial artery and arm microvascular function were determined by percent change of diameter from baseline normalized for BA shear rate (BAD/Shear), and blood flow area under the curve (BF AUC), respectively. Heart rate variability (HRV) was used to assess autonomic nervous system activity. Results: BF AUC was significantly lower (p = 0.02) and SNS activity was significantly higher (p = 0.02) in the PTSD group when compared to the CTRL group. BAD/Shear was not different between groups. Following the acute AO supplementation, BF AUC was augmented to which it was no longer significantly different (p = 0.16) when compared to the CTRL group. SNS activity within the PTSD group was significantly reduced (p=.007) following the AO supplementation when compared to the PL condition, and the difference between PTSD and CTRL was no longer significant (p=.41). Conclusion: Young individuals with PTSD demonstrated lower arm microvascular, but not brachial artery, function as well as higher sympathetic activity when compared to healthy controls matched for age, sex, and physical activity level. Furthermore, this microvascular dysfunction and SNS activity was attenuated by an acute AO supplementation to the level of the healthy controls. Taken together, this study revealed that the modulation of oxidative stress, via an acute AO supplementation, improved vascular dysfunction in individuals with PTSD, potentially by reducing the substantial SNS activity associated with this disorder.https://scholarscompass.vcu.edu/gradposters/1084/thumbnail.jp

Nonsteroidal Anti-Inflammatory Drugs and Ectodomain Shedding of the Amyloid Precursor Protein

Background: Epidemiological studies have suggested that long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with a reduced incidence of Alzheimer's disease (AD). Several mechanisms have been proposed to explain these findings including increased shedding of the soluble ectodomain of the amyloid precursor protein (sAPP), which functions as a neurotrophic and neuroprotective factor in vitro and in vivo. Objective: To clarify whether NSAIDs consistently stimulate sAPP secretion. Methods: 293-EBNA cells with stable overexpression of an APP-alkaline phosphatase fusion protein (APP-AP), SH-SY5Y and PC12 cells or primary telencephalic chicken neurons were treated with ibuprofen or indomethacin. APP shedding was then determined by measuring AP activity in conditioned media, Western blot analysis with antibodies against total sAPP or specific for sAPP-alpha, or in a pulse-chase paradigm. Results: AP activity in conditioned media was not increased after NSAID treatment of 293-EBNA cells whereas it was elevated by phorbol ester. Surprisingly, ibuprofen or indomethacin treatment of SH-SY5Y and PC12 cells expressing endogenous APP did not cause changes in sAPP or sAPP-alpha secretion or downregulation of cellular APP. These findings were further corroborated in primary chicken neuronal cultures. Conclusions: Using various experimental settings, we were unable to confirm sAPP or sAPP-alpha stimulation with the NSAIDs ibuprofen and indomethacin in transfected and nontransfected cells of neuronal and nonneuronal origin. Importantly, these findings seem to rule out chronic sAPP stimulation as an alternative mechanism of NSAID action in AD. Copyright (C) 2008 S. Karger AG, Base