Sympathetic Hyperfunction Causes Increased Sensitivity of the Autonomic Nervous System to Whole-Body X Irradiation

2005 ◽  
Vol 163 (2) ◽  
pp. 137-143 ◽  
Author(s):  
Mutsumi Matsuu ◽  
Kazuko Shichijo ◽  
Yuji Ikeda ◽  
Masahiro Ito ◽  
Shinji Naito ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Whole Body ◽  
Autonomic Nervous ◽  
X Irradiation ◽  
Increased Sensitivity

Distribution of the preferred clothing pressure over the whole body

2018 ◽  
Vol 89 (11) ◽  
pp. 2187-2198 ◽  
Author(s):  
Tamaki Mitsuno ◽  
Ayaka Kai
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Hydrostatic Pressure ◽  
Body Part ◽  
Whole Body ◽  
Elastic Band ◽  
Autonomic Nervous ◽  
Pressure Load ◽  
Calibration Methods ◽  
Clothing Pressure

A system for measuring clothing pressure employing a renewed hydrostatic pressure-balancing method was examined using three calibration methods. All methods revealed an almost perfectly linear Y = X relation for the pressure load (X) and the reading of the system (Y). In the application, the distributions of elastic band pressure were examined on 21 planes from head to foot. The preferred elastic band pressures of the leg and arm were significantly higher than those of the neck and abdomen. These results are due to the large presence of the autonomic nervous system at the surfaces of the neck and abdomen. In the area of the abdomen, the preferred elastic band pressure was higher from the mammilla to the shoulder than for the anteroposterior midlines. The development of compression ware must consider appropriate tightening for each body part.

scholarly journals Brain permeable AMPK activator R481 raises glycemia by autonomic nervous system activation and amplifies the counterregulatory response to hypoglycemia in rats

2019 ◽  
Author(s):  
Ana M. Cruz ◽  
Yasaman Malekizadeh ◽  
Julia M. Vlachaki Walker ◽  
Paul G. Weightman Potter ◽  
Katherine Pye ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Ventromedial Hypothalamus ◽  
Whole Body ◽  
Ampk Activation ◽  
Autonomic Nervous ◽  
Glucose Levels

ABSTRACTAMP-activated protein kinase (AMPK) is a critical cellular and whole body energy sensor activated by energy stress, including hypoglycemia, which is frequently experienced by people with diabetes. Previous studies using direct delivery of an AMPK activator to the ventromedial hypothalamus (VMH) in rodents increased hepatic glucose production. Moreover, recurrent glucoprivation in the hypothalamus leads to blunted AMPK activation and defective hormonal responses to subsequent hypoglycemia. These data suggest that amplifying AMPK activation may prevent or reduce frequency hypoglycemia in diabetes. We used a novel brain-permeable AMPK activator, R481, which potently increased AMPK phosphorylation in vitro. R481 significantly increased peak glucose levels during glucose tolerance tests in rats, which were attenuated by treatment with AMPK inhibitor SBI-0206965 and completely abolished by blockade of the autonomic nervous system. This occurred without altering insulin sensitivity measured by hyperinsulinemic-euglycemic clamps. Endogenous insulin secretion was not altered by R481 treatment. During hyperinsulinemic-hypoglycemic clamp studies, R481 treatment reduced exogenous glucose requirements and amplified peak glucagon levels during hypoglycemia. These data demonstrate that peripheral administration of the brain permeable AMPK activator R481 amplifies the counterregulatory response to hypoglycemia in rats, which could have clinical relevance for prevention of hypoglycemia.

Abstract P129: Role of the Autonomic Nervous System in Remote Postconditioning in Humans

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Rupert P Williams ◽  
Michael I Okorie ◽  
Harminder Gill ◽  
John E Deanfield ◽  
Raymond J MacAllister ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Whole Body ◽  
Limb Ischaemia ◽  
Protective Effects ◽  
Blood Pressure Cuff ◽  
Autonomic Nervous ◽  
Pressure Cuff ◽  
Remote Postconditioning

Brief periods of ischaemia activate systemic mechanisms that induce whole-body tolerance to subsequent prolonged and injurious ischaemia. This phenomenon, remote ischaemic preconditioning (RIPC), is sufficiently acute to reduce ischaemia-reperfusion (IR) injury even when applied simultaneously with injurious ischaemia. This aspect of RIPC is termed remote postconditioning (RPostC). We have previously demonstrated a role for the autonomic nervous system in RIPC. Using an in vivo model of endothelial IR injury, we determined if RPostC is dependent on adrenergic autonomic mechanisms. Vascular ultrasound was used to assess endothelial function in healthy volunteers by measuring dilatation of the brachial artery in response to increased blood flow during reactive hyperaemia (flow-mediated dilatation; FMD). Endothelial IR injury was induced by 20 min of upper limb ischaemia (inflation of a blood pressure cuff to 200 mm Hg) followed by reperfusion. RPostC was induced by applying 2 cycles of 5 minutes ischaemia and 5 minutes reperfusion on the leg during arm ischaemia (via a second blood pressure cuff). In order to determine the dependence of RPostC on autonomic activation, we administered the alpha adrenoceptor blocker phentolamine (0.2– 0.7mg/min, intravenously) during the application of the RPostC stimulus. FMD was determined before ischaemia and at 20 minutes of reperfusion. FMD (percentage change from baseline diameter) was compared statistically by ANOVA. IR alone caused a significant reduction in FMD (5.9±0.7% pre- versus 2.2±0.4% post-IR, n=9, P<0.001). This reduction was prevented by RPostC (5.8±0.4% pre- versus 5.4±0.3% post-IR, n=8, P>0.05). Systemic phentolamine blocked the protective effects of RPostC (FMD 6.1±0.5% pre- versus 2.0±0.3% post-IR, n=7, P<0.001). These data indicate, for the first time in humans, that protection from RPostC depends on preservation of adrenergic signalling. Alpha blockade neutralises one of the endogenous mechanisms of ischemic protection in humans; the clinical consequences of this remain to be determined.

scholarly journals Autonomic Nervous System Function in Newly Diagnosed Multiple Sclerosis: Association With Lipid Levels and Insulin Resistance

2021 ◽  
pp. 875-882
Author(s):  
M. Hardoňová ◽  
P. Šiarnik ◽  
M. Siváková ◽  
B. Suchá ◽  
M. Vlček ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Insulin Resistance ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Sympathetic Activity ◽  
Whole Body ◽  
Sensitivity Index ◽  
Positive Correlation ◽  
Autonomic Nervous ◽  
Significant Difference

Autonomic nervous system (ANS) disorders are common in multiple sclerosis (MS). Previous studies showed differences in insulin resistance (IR) and lipoprotein levels in MS subjects compared to controls. Lipolysis caused by increased sympathetic activity could be one of the possible linking mechanisms leading to dyslipidemia in MS. Our study aimed to evaluate ANS activity in the context of glucose and lipid metabolism in people with MS. We prospectively measured short-term heart rate variability (HRV), fasting lipoprotein concentrations, and calculated IR indices based on plasma glucose and insulin levels during oral glucose tolerance test (oGTT) in 32 patients with MS and 29 healthy controls matched for age, sex and body mass index in our study. There was no significant difference in HRV parameters and lipoprotein levels between MS and controls. A significant positive correlation was found between low/high-frequency power ratio (LF/HF) and triglycerides (r=0.413, p=0.021) in MS subjects but not in controls. A significantly lower whole-body insulin sensitivity index (ISIMat) was found in patients with MS compared to the control group (7.3±3.7 vs. 9.8±5.6, p=0.041). No significant correlations were found between LF/HF and IR parameters. In MS subjects, the positive correlation of LF/HF with triglycerides could reflect the effects of sympathetic activity on lipolysis. Positive correlations of sympathetic activity with increased lipoprotein levels could rather reflect processes associated with immune system activation/inflammation, than processes involved in glucose homeostasis maintenance.

Does the autonomic nervous system regulate whole-body lymph flow?

1983 ◽  
Vol 245 (5) ◽  
pp. R695-R700
Author(s):  
G. G. Power ◽  
R. A. Brace
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Isotonic Saline ◽  
Lymph Flow ◽  
Whole Body ◽  
Thoracic Duct Lymph ◽  
Ganglionic Blockade ◽  
Shed Blood ◽  
Autonomic Nervous

We compared whole-body lymph flow responses with and without the autonomic nervous system intact in pentobarbital-anesthetized, acutely nephrectomized dogs. We measured left thoracic duct lymph flow, lymph and plasma protein concentrations, arterial and venous pressures, heart rate, and hematocrit in eight intact and six ganglion-blocked (hexamethonium, 15 mg/kg iv) animals. Ganglionic blockade lowered arterial pressure and heart rate but did not change lymph flow rate or the other variables. In the control and blocked groups at 30-min intervals, isotonic saline, lactated Ringer, and Dextran 70 solutions were serially infused, followed by hemorrhage and reinfusion of shed blood. Infusions or withdrawals were equal to 2% of body weight and were induced over 5-min intervals followed by 25 min of recovery. Lymph flow generally increased to a peak 5–7 min after each infusion was ended and then decayed back toward preinfusion levels; the extent of the rise in lymph flow, the time of the peak flow, and the extent of decay after the peak were unaffected by autonomic blockade. The absolute lymph flow rates in response to the infusions, hemorrhage, or blood infusion were not appreciably altered by ganglionic blockade. Thus the present studies provide little support to the hypothesis that the autonomic nervous system contributes to whole-body lymph flow.

scholarly journals Autonomic nervous system activation mediates the increase in whole‐body glucose uptake in response to electroacupuncture

2017 ◽  
Vol 31 (8) ◽  
pp. 3288-3297 ◽  
Author(s):  
Anna Benrick ◽  
Milana Kokosar ◽  
Min Hu ◽  
Martin Larsson ◽  
Manuel Maliqueo ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Glucose Uptake ◽  
Whole Body ◽  
Autonomic Nervous ◽  
System Activation

Diseases of the autonomic nervous system

2010 ◽  
pp. 5055-5068
Author(s):  
Christopher J. Mathias ◽  
David A. Low
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Autonomic Control ◽  
Whole Body ◽  
Organ Function ◽  
Autonomic Nervous ◽  
System P ◽  
Efferent Pathways

The autonomic nervous system innervates all organs, producing predominantly involuntary and automatic actions that are mediated by two principal efferent pathways, the sympathetic and parasympathetic, which are neurochemically and anatomically distinct. Numerous synaptic relays and neurotransmitters allow the autonomic control of organ function at local and central levels to be integrated with the requirements of the whole body....

Whole body vascular capacitance response to vasopressin is mediated by autonomic function

1991 ◽  
Vol 261 (2) ◽  
pp. H493-H499 ◽  
Author(s):  
D. S. Martin ◽  
J. R. McNeill
Keyword(s):  
Nervous System ◽  
Cardiac Output ◽  
Autonomic Nervous System ◽  
Autonomic Function ◽  
Plasma Concentrations ◽  
Blocking Agent ◽  
Whole Body ◽  
Autonomic Nervous ◽  
Reservoir Volume ◽  
Vascular Capacitance

Effects of intravenous infusions of arginine vasopressin (AVP) on whole body vascular capacitance were determined in anesthetized cats when autonomic nervous system function was intact and, in other cats, when reflexes were blocked by the ganglionic blocking agent pentolinium. With the use of the constant cardiac output-reservoir technique, changes in reservoir volume were assumed to reflect reciprocal changes in whole body vascular capacitance. Relationships between the dose of AVP and the plasma concentration of the peptide achieved during infusions were not significantly different in the two groups of animals. Blood pressure responses to AVP were greater, whereas heart rate responses to the peptide were abolished in ganglion-blocked cats. In cats with intact autonomic function, reservoir volume decreased by 1.6, 4.2, and 7.8 ml/kg at AVP doses of 1, 10, and 100 ng.kg-1.min-1, respectively. In contrast, in ganglion-blocked cats, reservoir volume did not change significantly at 1.0 and 10 ng.kg-1.min-1 of AVP, and the highest dose caused a much smaller change in volume (3 ml/kg) than that observed in cats with intact autonomic function (7.8 ml/kg). Systemic compliance was unchanged by AVP in both groups of animals, suggesting that the increases in whole body vascular capacitance were likely due to changes in unstressed volume. The results suggest that reflexively mediated changes in autonomic function increase whole body vascular capacitance during elevations in the circulating levels of AVP to plasma concentrations that are biologically relevant. These findings may explain how AVP decreases cardiac output in animals with an intact autonomic nervous system.

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