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Nervous System Response (nervous + system_response)
Selected AbstractsBreastfeeding and Maternal Stress Response and HealthNUTRITION REVIEWS, Issue 7 2004Elizabeth Sibolboro Mezzacappa Ph.D. This article reviews findings on the maternal stress and health effects of lactation. Several significant associations have emerged. Compared with not breastfeeding, breastfeeding is associated with increased parasympathetic nervous system modulation, greater vascular stress response, lower perceived stress levels, and fewer depressive symptoms. Breastfeeding exclusively is associated with an attenuated initial sympathetic cardiac nervous system response to some laboratory stressors. Bottle-feeding is associated with increased sympathetic and decreased parasympathetic cardiac control. The act of breastfeeding is associated with decreased neuroendocrine response to stressors and decreased negative mood. Finally, breastfeeding is associated with enhanced physical and mental health compared with non-breastfeeding. [source] Functional alterations of mesenteric vascular bed, vas deferens and intestinal tracts in a rat hindlimb unloading model of microgravityAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 2 2004G. De Salvatore Summary 1 Prolonged bed rest or exposure to microgravity may cause several alterations in autonomic nervous system response (ANSR). 2 Hindlimb unloading (HU) rats were used as an animal model of simulated microgravity to investigate ANSR changes. The experiments were carried out to investigate the effects of simulated microgravity on the autonomic nervous response of the perfused mesenteric vascular bed (MVB), vas deferens and the colon and duodenum from 2-week HU rats. 3 In MVB preparations of HU rats, the frequency-dependent increases in perfusion pressure with perivascular nerve stimulation (PNS; 8,40 Hz) were inhibited, whereas the noradrenaline (NA) concentration-dependent (1,100 ,m) perfusion pressure increases were potentiated. The latter most probably reflected up-regulation of , -adrenergic receptor function. Relaxant responses of NA-precontracted MVB to PNS (4,30 Hz) or isoprenaline were not different between control and HU preparations, while vasodilation induced by the endothelial agonist ACh was reduced. 4 Transmural stimulation (2,40 Hz) induced frequency-dependent twitches of the vas deferens which were reduced in vas deferens of HU rats, while the sensitivity to NA-induced contraction was significantly increased. 5 In the gastroenteric system of HU rat, direct contractile responses to carbachol or tachykinin as well as relaxant or contractile responses to nervous stimulation appeared unchanged both in the proximal colon rings and in duodenal longitudinal strips. 6 In conclusion, HU treatment affects peripheral tissues in which the main contractile mediators are the adrenergic ones such as resistance vessels and vas deferens, probably by reducing the release of neuromediator. This study validates NA signalling impairment as a widespread process in microgravity, which may most dramatically result in the clinical phenotype of orthostatic intolerance. [source] Evidence for a vicious cycle of exercise and hypoglycemia in type 1 diabetes mellitusDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2004A. C. Ertl Abstract Exercise is a cornerstone of diabetes management as it aids in glycemic control, weight management, reducing blood pressure, and improving the quality of life of patients. Unfortunately, owing to the complexity and difficulties of regulating exogenous insulin in a physiologic manner during exercise, physical activity often results in hypoglycemia in patients with type 1 diabetes mellitus (type 1 DM). When glucose levels fall below threshold glycemic levels, neuroendocrine, autonomic nervous system (ANS), and metabolic glucose counterregulatory mechanisms are activated. These hypoglycemic counterregulatory mechanisms in type 1 DM can be blunted irreversibly by disease duration or by acute episodes of prior stress. These reduced (or absent) counterregulatory responses result in a threefold increase in severe hypoglycemia when intensive glycemic control is implemented in type 1 DM 1. Much recent work has been focused on determining the in vivo mechanisms responsible for causing the increased incidence of severe hypoglycemia in type 1 DM. Studies from several laboratories have demonstrated the role played by episodes of antecedent hypoglycemia in producing blunted glucose counterregulatory responses during subsequent exposures of hypoglycemia. Until recently, the mechanisms responsible for exercise related hypoglycemia in type 1 DM have been attributed to relative or absolute increases of insulin levels or incomplete glycogen repletion after physical activity. Owing to the qualitative similarity of neuroendocrine, ANS, and metabolic responses to hypoglycemia and exercise, we have hypothesized that neuroendocrine and ANS counterregulatory dysfunction may also play an important role in the pathogenesis of exercise-related hypoglycemia in type 1 DM. Vicious cycles can be created in type 1 DM, where an episode of hypoglycemia or exercise can feed forward to downregulate neuroendocrine and ANS responses to a subsequent episode of either stress, thereby creating further hypoglycemia (Figure 1). This article will review the recent work that has studied the contribution of counterregulatory dysfunction to exercise-induced hypoglycemia in type 1 DM. Copyright © 2004 John Wiley & Sons, Ltd. 1. Reciprocal vicious cycles may be created in type 1 diabetes mellitus (type 1 DM), whereby an episode of hypoglycemia or exercise can feed forward to downregulate neuroendocrine and autonomic nervous system responses to a subsequent episode of either stress, thereby creating further hypoglycemia [source] Stressor-induced modulation of immune function: a review of acute, chronic effects in animalsACTA NEUROPSYCHIATRICA, Issue 6 2002Alexander W. Kusnecov The present paper reviews recent studies on the effects of stress on immune function in laboratory animals. The emphasis is on those studies where a simultaneous comparison of acute and chronic stress regimens was determined, although additional relevant studies are also reviewed. The effects of stress on basic measurements of cellular and humoral immune measures are discussed, including the growing number of studies that have reported alterations in macrophage functions. The latter are key elements in the innate immune response, and like measurements of T cell function and antibody production, are inhibited and enhanced by stressor exposure. This review does not focus on the mechanisms by which stress alters immune function, there being little to add conceptually in terms of what was reported previously (see Kusnecov AW, Rabin BS, Int Arch Allergy Immunol 1994;105:107,121.). However, a question is raised in the conclusion as to how stressor effects on immune function should be interpreted, for it is clear that immunological processes in and of themselves elicit central nervous system responses that neurochemically and endocrinologically do not differ from those produced in response to psychological stressors. Therefore, at least in the short term stressor-induced immune changes may not necessarily reflect maladaptive adjustments, although, as demonstrated by some studies reviewed in this paper, they may pose a serious risk to health should stressor exposure be persistent and uncontrolled. [source] | ||||||||||