Thesis (M.A.)--Kent State University, 2008. / Title from PDF t.p. (viewed Oct. 15, 2009). Advisor: Joel Hughes. Keywords: PTSD, autonomic nervous system, parasympathetic nervous system, heart rate variability. Includes bibliographical references (p. 45-57).

Baroreflex control of heart rate (HR) is impaired in diabetes mellitus. We hypothesized that diabetes mellitus induced functional changes of neural components at multiple sites within the baroreflex arc. Type 1 diabetic mice (OVE26) and FVB control mice were anesthetized. Baroreflex-mediated HR responses to sodium nitroprusside- (SNP) and phenylephrine- (PE) induced mean arterial blood pressure (MAP) changes were measured. Baroreceptor function was characterized by measuring the percent (%) change of baseline integrated aortic depressor nerve activity (Int ADNA) in response to SNP- and PE-induced MAP changes. The HR responses to electrical stimulation of the left aortic depressor nerve (ADN) and the right vagus nerve were assessed. Compared with FVB control mice, we found in OVE26 mice that (1) baroreflex-mediated bradycardia and tachycardia were significantly reduced. (2) The baroreceptor afferent function in response to MAP increase did not differ, as assessed by the parameters of the logistic function curve. But, the inhibition of Int ADNA in response to MAP decrease was significantly attenuated. (3) The maximum amplitude of bradycardic responses to right vagal efferent stimulation was augmented. (4) In contrast, the maximum amplitude of bradycardic responses to left ADN stimulation was decreased. Since Int ADNA was preserved in response to MAP increase and HR responses to vagal efferent stimulation were augmented, we conclude that a deficit of the central mediation of baroreflex HR contributes to the overall attenuation of baroreflex sensitivity in OVE26 mice. The successful conduction of physiological experiments on the ADN in OVE26 mice may provide a foundation for the understanding of cellular and molecular mechanisms of diabetes-induced cardiac neuropathy.

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Neck-shoulder pain (NSP) is a highly prevalent musculoskeletal disorder with unclear causes, and effective prevention and treatment require a further understanding of the underlying mechanisms. Aberrant autonomic nervous system (ANS) regulation is a hypothesized causal element in the development and maintenance of chronic muscle pain. The overall aim of this thesis was to investigate possible differences in ANS regulation between chronic NSP and healthy control (CON) groups using both laboratory assessment and ambulatory monitoring in daily life. Four papers are included in this thesis, based on data from three groups with chronic NSP. Autonomic responses to laboratory stressors were assessed using heart rate variability (HRV), blood pressure, trapezius muscle activity and blood flow measurements (Study І) in NSP and CON. Long-term ambulatory monitoring of HRV, physical activity and perceived symptoms were assessed in Studies ІІ and IV to investigate group differences in real-life conditions. Finally, the effects of a ten-week intervention (using individually adjusted HRV biofeedback) to reinstating ANS balance in subjects with chronic NSP were evaluated using self-reported symptoms and health ratings, as well as autonomic regulation testing (i.e., evaluating HRV at rest and in response to stress) (Study ІІІ). The main findings from the four studies demonstrated aberrant ANS regulation in the NSP group compared to CON, which was predominantly characterized by diminished parasympathetic cardiac activity during rest and sleep, and altered sympathetic reactivity to laboratory stressors (Studies І, ІІ and IV). Different patterns in physical activity were observed between the NSP and CON groups, with reduced physical activity during leisure time in the NSP group (Studies ІІ and IV). Physical activity was found to be positively associated with HRV. Positive effects of HRV-biofeedback were found on perceived health, including social function, vitality and bodily pain, and improved HRV (Study ІІІ). In conclusion, imbalanced ANS regulation was demonstrated among persons with chronic NSP at both the systemic and local levels. Diminished parasympathetic activity in NSP was modulated by lower levels of physical activity in leisure time. Interventions targeting ANS functions might benefit persons with chronic NSP.

African Americans are at a greater risk of developing cardiovascular disease and associated risk factors than are Whites, and recent research has suggested that the effects of racial discrimination are a significant contributor to this disparity. Thus, a preattentive bias and vigilance for threat might serve as a mechanism through which experienced racial discrimination would negatively impact cardiovascular health. A study was conducted to investigate the physiological and attentional underpinnings of vigilance for discriminatory threat via examination of phasic heart period (HP) responses to cued threat and nonthreat stimuli. Thirty African American and forty-two European American undergraduate students from a large urban university participated in the study. Phasic HP reactions of participants were recorded during an S1-S2 procedure where cued stereotype-related threatening, nonstereotype-related threatening, and nonthreatening stimuli were presented. It was hypothesized that Blacks, more than Whites, would show: smaller magnitude and impaired habituation of cardiac orienting to neutral words; acceleration of heart rate in response to threat words; and a conditioned anticipatory heart rate deceleration to threat words over repeated trials. However, results did not support hypotheses; neither Whites nor Blacks exhibited significant changes in phasic heart period in response to cued stimuli.

Dissertation (Ph.D.)--University of Toledo, 2009. / "In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 138-150.

abstract: The objective of this study was to examine the potential effects of long term hormone replacement therapy on cardiovascular autonomic nervous system responses to laboratory social stressors. The participants were 38 postmenopausal women, 18 using estrogen and progesterone hormone replacement therapy for at least 2 years and 20 control participants without hormone replacement therapy. All women completed orthostasis (standing and sitting), then speech and math tasks (speech and math were counterbalanced). Cardiovascular measures of sympathetic nervous system (pre-ejection period, PEP) and parasympathetic nervous system (respiratory sinus arrhythmia, RSA) along with heart rate were collected throughout all periods (baseline, orthostasis, and stressors). For orthostasis, results of mixed analyses of variance (ANOVAs) showed expected period effects for heart rate, RSA and PEP, but no group or group by period interaction was significant. For the psychological stressors, period main effects were significant for all three variables, suggesting that the tasks were effective at inducing stress. Also, there was a significant interaction between group and period for RSA, demonstrated by greater decrease during the psychological stressor period in the group using HRT. The interactions between group and period for heart rate and PEP were non-significant. These findings support the notion that HRT may slow age-related decreases in parasympathetic responsiveness. Furthermore, changes in vagal reactivity in relation to use of HRT appear to occur within mechanisms involving response and coping with psychological stressors, rather than mechanisms that accommodate basic physiological task such as orthostasis. / Dissertation/Thesis / M.S. Psychology 2013

Intrinsic cardiac neurons are core elements of a complex neural network that serves as an important integrative center for regulation of cardiac function. Although mouse models are used frequently in cardiovascular research, very little is known about mouse intrinsic cardiac neurons. Accordingly, we have dissociated neurons from adult mouse heart, maintained these cells in culture, and defined their basic phenotypic properties. Neurons in culture were primarily unipolar, and 89% had prominent neurite outgrowth after 3 days (longest neurite length of 258 ± 20 μm, n = 140). Many neurites formed close appositions with other neurons and nonneuronal cells. Neurite outgrowth was drastically reduced when neurons were kept in culture with a majority of nonneural cells eliminated. This finding suggests that nonneuronal cells release molecules that support neurite outgrowth. All neurons in coculture showed immunoreactivity for a full complement of cholinergic markers, but about 21% also stained for tyrosine hydroxylase, as observed previously in sections of intrinsic cardiac ganglia from mice and humans. Whole cell patch-clamp recordings demonstrated that these neurons have voltage-activated sodium current that is blocked by tetrodotoxin and that neurons exhibit phasic or accommodating patterns of action potential firing during a depolarizing current pulse. Several neurons exhibited a fast inward current mediated by nicotinic ACh receptors. Collectively, this work shows that neurons from adult mouse heart can be maintained in culture and exhibit appropriate phenotypic properties. Accordingly, these cultures provide a viable model for evaluating the physiology, pharmacology, and trophic factor sensitivity of adult mouse cardiac parasympathetic neurons.

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No description available.