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<p>  </p> <p>Persons with a spinal cord injury (SCI) often suffer from secondary complications including the dysfunction of the autonomic nervous system below the level of injury. For persons with a SCI at or above T6, autonomic dysreflexia (AD) may be triggered by noxious stimulation below the level of injury causing rapid sympathetic hyperactivation, leading to paroxysmal hypertension. If AD is not recognized and managed promptly, this increase in blood pressure can lead to stroke, organ damage, and/or death. Currently, AD is only detected in clinical settings through continuous blood pressure monitoring. Recent studies have revealed that rapid detection of AD is possible by using extracted features from electrocardiogram (ECG) data collected non-invasively and applying a five-layer neural network.</p> <p>This project focuses on further characterization of physiological responses before and during AD to detect the overreaction of sympathetic nerve activity prior to the detrimental increase in hypertension. Using a rat model with implanted telemetry and noninvasive sensors, an acclimation protocol was developed to minimize noise and motion artifacts during data collection. We induced AD in a controlled manner using colorectal distention (CRD). We analyzed skin nerve activity (SKNA) and heart rate variability parameters in the time and frequency domain to improve the non-invasive detection of AD. A four-week acclimation protocol exposed a minimal increase in sympathetic activity during experimentation despite long periods of restraint. Results indicated an increase in SKNA features occurred about 18 seconds before the gold standard increase in blood pressure. Additionally, integrated SKNA features in the frequency domain quantified nerve activity and low frequency components were found to be dominant during AD, providing another parameter that could be included in an AD detection system to improve accuracy. In humans, SKNA may be used to alert patients of the onset of AD, allowing caretakers to respond quickly and make necessary changes to decrease the severe effects of AD.</p>

The purpose of this investigation was to examine the potential differences in autonomic nervous system adaptations, as assessed by heart rate variability techniques, between a group of stabilized CHF patients randomized to either a training group (aerobic+resistance) or a control group (usual care). In a single-blind, randomized controlled trial of 3-months of supervised exercise training and a further 3-months of home-based exercise, 28 stabilized CHF patients (NYHA 1-111) were randomized to either a training (AERWT) (n=16;11M,5F; age, 64.9±2.3; LVEF, 29.4±1.7%) or usual care (UC) (n=12; 10M,2F; age, 58.0±2.8; LVEF, 24.4±2.0%) group. Upon completion of the supervised exercise program, the AERWT group increased peak oxygen uptake (V02) (13.2±0.5 to 15.5±0.84 ml/kg/min, p<0.05), and single-arm curl scores (16.2±2.8 to 19.2±3.3 kg, p<0.05) significantly compared to the UC group, without any deleterious effect upon clinical status or left-ventricular function (LVEF: 31.3±1.7 to 33.2±1.9%, p=0.99). Physical training reduced expired ventilation and carbon dioxide based on successive workloads during symptom-limited incremental cycle ergometry in the AERWT group; however, this was found to be non-significant, in addition to changes in resting heart rate, anaerobic threshold, maximal exercise duration, maximal power output, and double product following training. Supine, resting power spectral indices remained unchanged from baseline to 6-months in both groups, as did the recovery of power spectral indices during supine rest following a symptom-limited incremental cycle ergometry test. A qualitative comparison of the power spectral changes from supine to standing revealed no significant differences between groups with respect to improvements in the baroreceptor response to orthostatic stress. Time domain parameters, derived from 24-hour ambulatory bolter monitoring, were also obtained at baseline, 3-months, and 6-months. The indices believed to be largely representative of vagal modulation, SDNN-Index, r-MSSD, and pNN50, tended to increase in the AERWT group with increased participation in the training program; however, the results did not obtain statistical significance (p=0.07). In addition, there were no significant changes in mean 24-hour heart rate or NN-interval, SDNN, or SDANN in the AERWT group (p=0.21). The present investigation revealed some evidence to suggest that exercise training in selected populations of CHF patients results in favourable changes in vagal modulation and baroreceptor sensitivity; however, unlike Coats et al. (1992), the present investigation failed to note any significant alterations in HRV frequency domain indices as a result of exercise training despite identical improvements in peak V02. The lack of significant findings in both the frequency and time domain HRV data could indicate that the autonomic dysfunction is so widespread and rampant in CHF that we cannot induce alterations through training as would be demonstrated in normal, healthy controls. In effect, these findings reinforce the hypothesis that in CHF the heart is the 'slave' of the periphery, and that due to the progressive lack of neural control of both the heart and circulation, in addition to an impairment in pump function, that the only effective means of improving physiological variables is through changes at the peripheral level. / Thesis / Master of Science (MS)

Obesity is associated with sympathetic neural activation and elevated blood pressure(1,2). However, it is unclear whether modest elevations in body weight are sufficient to induce increases sympathetic activity (3). Furthermore, there is a large amount of individual variability in the blood pressure response to weight change (4). The reason(s) for this inter-individual variability are still uncertain, but body fat distribution and cardiorespiratory fitness may play a role (5,6). To address these and other issues regarding the relation between adiposity, sympathetic neural activity and blood pressure, we first examined the effects of modest, diet-induced weight gain on muscle sympathetic nervous system activity (MSNA) in healthy, lean, normotensive individuals. We hypothesized that modest weight gain would increase MSNA in these individuals, and that this neural activation would be accompanied by increases in blood pressure. Concordant with this hypothesis, MSNA and resting blood pressure were significantly elevated following weight gain. The increase in MSNA was correlated with the magnitude of body weight and fat gain, but was not obviously related to increases in visceral fat. We next examined the ability of cardiorespiratory fitness (CRF) to modulate the weight gain-induced increase in blood pressure in the same cohort of young, nonobese and normotensive individuals. We hypothesized that the increase in blood pressure would be attenuated in individuals with higher- compared with lower CRF (HCRF and LCRF, respectively). Indeed, we found that HCRF experienced significantly smaller increases in resting and ambulatory blood pressure compared to LCRF. In the pooled sample, baseline fitness was inversely related to the changes in resting systolic and diastolic pressure, and this relation was not diminished after statistically controlling for changes in abdominal visceral fat. The results of the present investigation suggest that even modest weight gain increases sympathetic activity and blood pressure, which, if left untreated, may contribute to the development of hypertension and other cardiovascular disorders. Maintenance of higher levels of CRF during periods of weight gain may reduce cardiovascular disease risk by mitigating the increases in blood pressure. Collectively, these findings may have important implications for understanding the link between obesity and hypertension. References 1. Davy KP. The global epidemic of obesity: are we becoming more sympathetic? Curr Hypertens Rep. 2004;6:241-6. 2. Grassi G, Seravalle G, Cattaneo BM, et al. Sympathetic activation in obese normotensive subjects. Hypertension. 1995;25:560-3. 3. Huggett RJ, Scott EM, Gilbey SG, Bannister J, Mackintosh AF, Mary DA. Disparity of autonomic control in type 2 diabetes mellitus. Diabetologia. 2005;48:172-9. 4. Masuo K, Mikami H, Ogihara T, Tuck ML. Weight gain-induced blood pressure elevation. Hypertension. 2000;35:1135-40. 5. Hayashi T, Boyko EJ, Leonetti DL, et al. Visceral adiposity is an independent predictor of incident hypertension in Japanese Americans. Ann Intern Med. 2004;140:992-1000. 6. Barlow CE, LaMonte MJ, Fitzgerald SJ, Kampert JB, Perrin JL, Blair SN. Cardiorespiratory fitness is an independent predictor of hypertension incidence among initially normotensive healthy women. Am J Epidemiol. 2006;163:142-50. / Ph. D.

No / Purpose: Evidence exists for an additional inhibitory accommodative control system mediated by the sympathetic branch of the autonomic nervous system (ANS). This work aims to show the relative prevalence of sympathetic inhibition in young emmetropic and myopic adults, and to evaluate the effect of sympathetic facility on accommodative and oculomotor function. Methods: Profiling of ciliary muscle innervation was carried out in 58 young adult subjects (30 emmetropes, 14 early onset myopes, 14 late onset myopes) by examining post-task open-loop accommodation responses, recorded continuously by a modified open-view infrared optometer. Measurements of amplitude of accommodation, tonic accommodation, accommodative lag at near, AC/A ratio, and heterophoria at distance and near were made to establish a profile of oculomotor function. Results: Evidence of sympathetic inhibitory facility in ciliary smooth muscle was observed in 27% of emmetropes, 21% of early-onset myopes and 29% of late-onset myopes. Twenty-six percent of all subjects demonstrated access to sympathetic facility. Closed-loop oculomotor function did not differ significantly between subjects with sympathetic facility, and those with sympathetic deficit. Conclusions: Emmetropic and myopic groups cannot be distinguished in terms of the relative proportions having access to sympathetic inhibition. Presence of sympathetic innervation does not have a significant effect on accommodative function under closed-loop viewing conditions.

Baroreflex function and cardiovascular responses to lower body negative pressure during selective autonomic blockade were evaluated in endurance exercise trained (ET) and untrained (UT) men. Baroreflex function was evaluated using a progressive intravenous infusion of phenylephrine HCL (PE) to a maximum of 0.12 mg/min. Heart rate, arterial blood pressure, cardiac output and forearm blood flow were measured at each infusion rate of PE. The reduction in forearm blood flow and concomitant rise in forearm vascular resistance was the same for each subject group. However, the heart rate decreases per unit increase of systolic or mean blood pressure were significantly (P<.05) less in the ET subjects (0.91 ± 0.30 versus 1.62 ± 0.28 for UT). During progressive lower body negative pressure with no drug intervention, the ET subjects had a significantly (P<.05) greater fall in systolic blood pressure (33.8 ± 4.8 torr versus 16.7 ± 3.9 torr). However, the change in forearm blood flow or resistance was not significantly different between groups. Blockade of parasympathetic receptors with atropine (0.04 mg/kg) eliminated the differences in response to lower body negative pressure. Blockade of cardiac sympathetic receptors with metoprolol (0.02 mg/kg) did not affect the differences observed during the control test. It was concluded that the ET subjects were less effective in regulating blood pressure than the UT subjects, because of 1) an attenuated baroreflex sensitivity, and 2) parasympathetic-mediated depression of cardiac and vasoconstrictive responses to the hypotensive stress.

Thesis (M.Ost.)--Unitec New Zealand, 2008. / Includes bibliographical references (leaves 92-99).

Individual differences in autonomic nervous system responsiveness have been linked to a variety of physical disorders and personality and behavioral tendencies. The present study attempted to correlate specific personality characteristics hypothesized to be associated with either sympathetic or parasympathetic dominance based on the work of M. A. Wenger. The Clinical Analysis Questionnaire Personality Inventory, a physical disorders questionnaire, a self-report stress measure, and seven psychophysiologic tests were administered to 60 undergraduate students in an introductory psychology class at North Texas State University. The results provided limited support for the hypotheses. A skewed population with 50 of the 60 subjects achieving scores indicative of sympathetic dominance occurred. Statistical comparison (t-tests) of the CAQ personality traits, and clinical factor scores of these 50 subjects labeled sympathetic dominant with CAQ norms for college students revealed means on five personality traits and three clinical factors were significantly different for the sympathetic dominant group at the .05 or greater level of significance. These findings were interpreted as limited support for Wenger's work and for the positions of Acker and Kagan that individuals with more reactive sympathetic nervous systems tend to have difficulty binding anxiety, poor emotional controls and outlets, ambivalence about interpersonal relationships, and a need for group acceptance.

Kwok, Ka Ming. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 124-146). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS --- p.i / ABSTRACT / In English --- p.ii / In Chinese --- p.v / LIST OF TABLES --- p.vii / LIST OF FIGURE --- p.ix / ABBREVIATIONS / For Units --- p.x / For Prefixes of the International System of Units --- p.x / For Terms Commonly Used --- p.xi / Role of research workers --- p.xv / Chapter CHAPTER 1 --- Overview of methylmercury / Chapter 1.1 --- Source of methylmercury --- p.1 / Chapter 1.2 --- Toxicokinetics --- p.3 / Chapter 1.2.1 --- Absorption and distribution --- p.3 / Chapter 1.2.2 --- Half-life --- p.5 / Chapter 1.2.3 --- Metabolism/Biotransformation --- p.5 / Chapter 1.2.4 --- Biochemical mechanism of toxicity --- p.7 / Chapter 1.3 --- Health effects of mercury exposure --- p.9 / Chapter 1.3.1 --- Adult central nervous system --- p.10 / Chapter 1.3.2 --- The developing central nervous system --- p.11 / Chapter 1.3.3 --- Cardiovascular effects --- p.13 / Chapter 1.3.4 --- Immunotoxicity --- p.14 / Chapter 1.4 --- Biomarkers for prenatal exposure --- p.15 / Chapter 1.5 --- MeHg exposure in high risk populations in Hong Kong --- p.17 / Chapter CHAPTER 2 --- Neurocognitive performance / Chapter 2.1 --- Introduction --- p.19 / Chapter 2.1.1 --- New Zealand --- p.20 / Chapter 2.1.2 --- Seychelles --- p.21 / Chapter 2.1.3 --- Faroe Islands --- p.22 / Chapter 2.1.4 --- The Hong Kong situation --- p.23 / Chapter 2.2 --- Method --- p.23 / Chapter 2.2.1 --- Subjects and study design --- p.23 / Chapter 2.2.2 --- Questionnaires --- p.24 / Chapter 2.2.3 --- Hg concentration measurement --- p.25 / Chapter 2.2.4 --- Neurocognitive measurements --- p.26 / Chapter 2.2.4.1 --- Hong Kong - Wechsler Intelligence Scale for Children --- p.27 / Chapter 2.2.4.2 --- Hong King List Learning Test --- p.28 / Chapter 2.2.4.3 --- Test of Everyday Attention for Children --- p.29 / Chapter 2.2.4.4 --- Boston Naming Test --- p.31 / Chapter 2.2.4.5 --- Grooved Pegboard Test --- p.31 / Chapter 2.2.5 --- Statistical analysis --- p.32 / Chapter 2.3 --- Results --- p.33 / Chapter 2.3.1 --- Subject characteristic --- p.33 / Chapter 2.3.2 --- Test results --- p.34 / Chapter 2.3.3 --- Statistical analysis results --- p.35 / Chapter 2.4 --- Discussion --- p.36 / Chapter CHAPTER 3 --- Cardiac autonomic function / Chapter 3.1 --- Introduction --- p.60 / Chapter 3.1.1 --- Mechanism --- p.60 / Chapter 3.1.2 --- The association between HRV and the ANS --- p.61 / Chapter 3.1.3 --- Clinical applications and related studies --- p.63 / Chapter 3.1.4 --- Associations between MeHg exposure & HRV --- p.64 / Chapter 3.2 --- Methods --- p.65 / Chapter 3.2.1 --- Subjects and study design --- p.65 / Chapter 3.2.2 --- Physical and HRV measurement --- p.66 / Chapter 3.2.3 --- Time domain analysis --- p.68 / Chapter 3.2.4 --- Frequency domain analysis --- p.68 / Chapter 3.2.5 --- Non-linear method --- p.69 / Chapter 3.2.6 --- Statistical analysis --- p.70 / Chapter 3.3 --- Results --- p.71 / Chapter 3.3.1 --- Subjects characteristics --- p.71 / Chapter 3.3.2 --- HRV and statistical analysis results --- p.71 / Chapter 3.4 --- Discussion --- p.73 / Chapter CHAPTER 4 --- Immuno-toxicity / Chapter 4.1 --- Introduction --- p.91 / Chapter 4.2 --- Methods --- p.96 / Chapter 4.2.1 --- Subjects and Study Design --- p.96 / Chapter 4.2.2 --- Cytokine measurement --- p.96 / Chapter 4.2.3 --- Reversibility --- p.98 / Chapter 4.2.4 --- Statistical Analysis --- p.99 / Chapter 4.3 --- Results --- p.101 / Chapter 4.3.1 --- Subject Characteristics --- p.101 / Chapter 4.3.2 --- Atopic and non-atopic diseases group --- p.101 / Chapter 4.3.3 --- Cytokine profiles --- p.102 / Chapter 4.3.4 --- Reversibility --- p.103 / Chapter 4.4 --- Discussion --- p.104 / Chapter CHAPTER 5 --- Conclusion --- p.119 / Reference List --- p.124