Browsing by Subject "autonomic"
Now showing 1 - 2 of 2
- Results Per Page
- Sort Options
Item Dysfunctional neuroimmune pathways promote the development and maintenance of lupus hypertension(2020-05) Pham, Grace S.; Mathis, Keisa W.; Rickards, Caroline A.; Goulopoulou, Styliani; Cunningham, J. Thomas; Ma, Rong; Mathew, Stephen O.Hypertension afflicts nearly half of the adults in the United States and the majority of cases have no known cause. Chronic inflammation has been implicated in the development and maintenance of hypertension, and autoimmunity may comprise one of its sources. Hypertension is highly prevalent in the autoimmune disease systemic lupus erythematosus (SLE), in which chronic aberrant inflammation may be a causative factor. Endogenous neuroimmune pathways, such as the hypothalamic-pituitary-adrenal (HPA) axis and the cholinergic anti-inflammatory pathway, likely contribute to this phenomenon. The HPA axis is a classical neuroimmune mechanism that senses peripheral inflammation via afferent vagal fibers, culminating in the release of the anti-inflammatory hormone cortisol. Previous studies have characterized HPA axis dysfunction in SLE, but less is known about how this dysregulation specifically impacts the hypertension that occurs in the setting of SLE. A second neuroimmune interaction, the cholinergic anti-inflammatory pathway, is an efferent vagus nerve-to-spleen mechanism that relies on T cell-produced acetylcholine to quell inflammation in acute settings and may be hypoactive in chronic inflammatory diseases like SLE. Notably, both of these neuroimmune mechanisms depend on vagus nerve function, identifying the vagus as a potential target for neuromodulation. Furthermore, the relationship between chronic inflammation and hypertension validates the investigation of neuroimmune pathway dysfunction towards novel mechanisms of hypertension. Herewithin, the HPA axis and cholinergic anti-inflammatory pathway are investigated using the well-established NZBWF1 mouse model of lupus hypertension. Our findings are that (1) administration of an inflammatory stimulus that activates vagal afferents elicits comparable neuronal activation in the paraventricular nucleus of the hypothalamus, compared to control mice, despite heightened peripheral inflammation; (2) amplification of efferent vagus nerve activity reduces blood pressure and renal inflammation; and (3) chronic unilateral vagotomy paradoxically results in decreased blood pressure and renal inflammation. Taken together, these findings identify dysfunction in two neuroimmune pathways while demonstrating that interventions targeting these pathways may have therapeutic benefits in lupus hypertension. In terms of future impact, these results may promote continuing inquiry in a more recently discovered neuroimmune pathway (i.e., cholinergic anti-inflammatory pathway), as well as reinstate curiosity in an older, abandoned area of research (i.e., HPA).Item Osteopathic Manipulative Medicine in Pregnancy: Acute Physiological and Biomechanical Effects(2009-05-01) Hensel, Kendi L.; Smith, Michael L.Introduction: During pregnancy, a woman’s body is challenged by significant physiological and biomechanical changes which can adversely affect normal function, mobility and quality of life. These changes may also contribute to co-morbid conditions accompanying pregnancy. Osteopathic manipulative medicine (OMM) is theorized to facilitate the body’s adjustment to the physiological and biomechanical demands of pregnancy and improve the outcomes of pregnancy, labor and delivery. Thus, this dissertation research was designed to examine the possible effects of an acute regimen of OMM on the autonomic and hemodynamic control mechanisms and gait and mobility function in women during the third trimester of pregnancy. Methods: Two studies were performed with 60 women at the 30th week of pregnancy. Study 1: The hemodynamic and autonomic (heart rate variability) responses to head-up tilt with and without engagement of the muscle pump via toe raising were assessed before and after a regimen of either randomly assigned OMM, sub-therapeutic placebo ultrasound, or a timecontrol. Study 2: Assessment of a cadre of gait parameters and functions was performed before and after application of the same randomized treatment regimens. Results: In Study 1, the response to tilt was not affected by OMM or placebo ultrasound, however, the systolic blood pressure response to toe raising was increased after OMM and was accompanied by a lower heart rate and enhanced vagal control of heart rate. In study 2, there were no statistically significant differences between groups at baseline. In addition, there were no statistically significant differences between pre-and post-treatment values for any spatiotemporal gait parameters. However, improvements in stride width and base of support trended toward significance. Conclusions: These data suggest that OMM improved hemodynamic control during engaging of the skeletal muscle pump that was most likely due to improvement of structural impediments to venous return. The gait data fail to elucidate a significant effect of OMM on gait parameters during the third trimester of pregnancy.