Responses of sympathetic nervous system to cold exposure in vibration syndrome subjects and age-matched healthy controls

1990 ◽  
Vol 62 (2) ◽  
pp. 177-181 ◽  
Author(s):  
Minoru Nakamoto
1983 ◽  
Vol 245 (2) ◽  
pp. E148-E154 ◽  
Author(s):  
J. B. Young ◽  
L. Landsberg

The genetically obese (ob/ob) mouse exhibits defective thermoregulatory responses to cold exposure. Pathophysiological explanations for this phenomenon have focused on abnormalities in intracellular metabolism or insensitivity of peripheral tissues to the thermogenic effects of catecholamines. Because the sympathetic nervous system (SNS) is subject to feedback regulation, a peripheral impairment in thermogenesis should be associated with a compensatory increase in SNS activity. To examine SNS activity in the ob/ob mouse, norepinephrine (NE) turnover was measured in heart and interscapular brown adipose tissue (IBAT) of ob/ob and lean mice. The results from studies utilizing radiolabeled NE or inhibition of NE biosynthesis with alpha-methyl-p-tyrosine to measure NE turnover demonstrated reductions in SNS activity of 33-56% in heart and of 45-73% in IBAT in ob/ob mice at ambient temperature (22 degrees C) compared with measurements in lean controls. During cold exposure (4 degrees C) NE turnover increased in heart and IBAT to a similar extent in both ob/ob and lean mice, but NE turnover rates in heart, and probably in IBAT as well, remained lower in the obese mice than in the lean despite the gradual development of hypothermia in the ob/ob mice during this period. Administration of naltrexone, a long-acting opiate antagonist, failed to reverse the suppression of SNS activity observed in the ob/ob mice. These data indicate that diminished SNS activity in ob/ob mice may be an additional factor contributing to the defective thermogenesis characteristic of these animals.


2019 ◽  
Vol 3 (s1) ◽  
pp. 55-55
Author(s):  
Jordan L Schultz ◽  
Lyndsay Harshman ◽  
John Kamholz ◽  
Peggy Nopoulos

OBJECTIVES/SPECIFIC AIMS: This study (1) investigated the presence and severity of autonomic nervous system (ANS) dysfunction in patients with pre-symptomatic Huntington Disease (HD) and (2) determined if pharmacologic manipulation of the ANS could modify the progression of HD. METHODS/STUDY POPULATION: Using a unique data set of children at-risk for HD (the Kids-HD study), markers of autonomic function (resting heart rate [rHR], blood pressure [BP], and core body temperature [CBT]) were compared between pre-symptomatic, gene-expanded children (psGE) and healthy developing children using mixed models analyses controlling for sex, age, and body mass index. Included participants had to be < 18 years old and be at least 10 years from their predicted motor diagnosis of HD. Using the Enroll-HD database, inverse-propensity score weighted, Cox Regression analyses investigated the effects of beta-blockers on the timing of motor diagnosis of presymptomatic, adult patients with HD. RESULTS/ANTICIPATED RESULTS: Compared to healthy controls, the psGE participants had significantly (p<0.05) higher mean rHR, systolic BP percentile, and CBT compared to the healthy controls (elevated by 4.01 bpm 0.19°C, and 5.96 percentile points, respectively, in the psGE group). Participants from Enroll-HD who were using a beta-blocker prior to motor diagnosis (n=65) demonstrated a significantly lower annualized risk of motor diagnosis [HR=0.56, p=0.03], compared to other participants with HD (n=1972). DISCUSSION/SIGNIFICANCE OF IMPACT: Sympathetic nervous system activity is elevated in patients with HD decades prior to their predicted motor diagnosis. Furthermore, modulation of the sympathetic nervous system with beta-blockers significantly lowers the annualized risk of motor diagnosis of HD.


1999 ◽  
Vol 77 (4) ◽  
pp. 250-258 ◽  
Author(s):  
Alicia M Passerin ◽  
Linda L Bellush ◽  
William N Henley

In a four-part study, we expand on our previous report that bulbospinal serotonin (5HT) neuronal activation occurs with 24 h of cold exposure. To characterize temporal aspects, rats were exposed to 3°C or were maintained at 22°C for 2, 8, 48, or 96 h (experiment 1) or for 15, 30, or 60 min (experiment 2). To ensure that cold-induced changes in 5HT activity were not due to disturbances in diurnal pattern, rats in experiment 3 were exposed to cold (8 h) during the dark cycle. To explore the hypothesis that cold-induced 5HT activation is part of a broad metabolic response that includes activation of the sympathetic nervous system, metabolically impaired (hypothyroid) rats were exposed to 8°C in experiment 4. Significant increments in 5-hydroxyindoleacetic acid (5HIAA) concentration were evident by 60 min of cold exposure and existed at all later time points measured. These findings were most robust in spinal cord and rostral brainstem. Activation in spinal cord was also found when rats were exposed to 8 h of cold during the dark cycle, the active period for rats. In experiment 4, hypothyroid rats exhibited significantly greater norepinephrine excretion compared with control rats exposed to the same cold stimulus; this finding was accompanied by significantly greater increments in 5HIAA concentration in rostral brainstem and spinal cord of hypothyroid rats. In addition, significant elevations in tryptophan concentration were noted throughout the brainstem and spinal cord of cold-exposed, hypothyroid rats relative to room temperature, hypothyroid rats. This finding suggested that elevations in 5HIAA concentration in these rats were due to increases in precursor availability. The implications of these findings relative to autonomic and metabolic control are discussed.Key words: serotonin, spinal cord, raphe, cold, sympathetic nervous system.


2019 ◽  
Vol 133 (9) ◽  
pp. 1097-1113 ◽  
Author(s):  
Ken Chen ◽  
Dongdong Sun ◽  
Shuang Qu ◽  
Yue Chen ◽  
Jialiang Wang ◽  
...  

Abstract Environmental temperature plays a role in the variation of blood pressure. Maternal cold stress could affect the physiological phenotype of the offspring, including blood pressure elevation. In the present study, we found that adult offspring of dams exposed to cold have increased systolic and diastolic blood pressure, and decreased urine volume and sodium excretion, accompanied by increased heart rate and heart rate variability, secondary to increased activity of the sympathetic nervous system. Renal denervation or adrenergic receptor blockade decreased blood pressure and increased sodium excretion. The increase in peripheral sympathetic nerve activity can be ascribed to the central nervous system because administration of clonidine, a centrally acting α2 adrenergic receptor agonist, lowered blood pressure to a greater degree in the prenatal cold-exposed than control offspring. Moreover, these prenatal cold-exposed offspring had hypothalamic paraventricular nucleus (PVN) disorder because magnetic resonance spectroscopy showed decreased N-acetylaspartate and increased choline and creatine ratios in the PVN. Additional studies found that prenatal cold exposure impaired the balance between inhibitory and excitatory neurons. This led to PVN overactivation that was related to enhanced PVN-angiotensin II type 1 (AT1) receptor expression and function. Microinjection of the AT1 receptor antagonist losartan in the PVN lowered blood pressure to a greater extent in prenatal cold-exposed that control offspring. The present study provides evidence for overactive peripheral and central sympathetic nervous systems in the pathogenesis of prenatal cold-induced hypertension. Central AT1 receptor blockade in the PVN may be a key step for treatment of this type hypertension.


Author(s):  
Erik Boberg ◽  
Ellen Iacobaeus ◽  
Myrto Sklivanioti Greenfield ◽  
Yanlu Wang ◽  
Mussie Msghina ◽  
...  

AbstractLong-term fatigue and cognitive dysfunction affects 35% of allogeneic haematopoietic stem cell transplantation (aHSCT) survivors, suggesting a dysfunctional prefrontal cortex. In this study, we assessed prefrontal cortex and sympathetic nervous system activity in aHSCT patients with fatigue (n = 12), non-fatigued patients (n = 12) and healthy controls (n = 27). Measurement of near-infrared spectroscopy and electrodermal activity was carried out at rest and during cognitive performance (Stroop, verbal fluency and emotion regulation tasks). Prefrontal cortex and sympathetic nervous system activity were also analyzed in response to dopamine and noradrenaline increase after a single dose of methylphenidate. Baseline cognitive performance was similar in the two patient groups. However, after methylphenidate, only non-fatigued patients improved in Stroop accuracy and had better verbal fluency task performance compared to the fatigued group. Task-related activation of prefrontal cortex in fatigued patients was lower compared to non-fatigued patients during all cognitive tests, both before and after methylphenidate administration. During the Stroop task, reaction time, prefrontal cortex activation, and sympathetic nervous system activity were all lower in fatigued patients compared to healthy controls, but similar in non-fatigued patients and healthy controls.Reduced prefrontal cortex activity and sympathetic arousal suggests novel treatment targets to improve fatigue after aHSCT.


2021 ◽  
Vol 10 (16) ◽  
pp. 3565
Author(s):  
Lisa Goudman ◽  
Nieke Vets ◽  
Julie Jansen ◽  
Ann De Smedt ◽  
Maxime Billot ◽  
...  

Despite the well-known clinical effects of spinal cord stimulation (SCS), the mechanisms of action have not yet been fully unraveled. The primary aim of this study was to measure whether electrochemical skin conductance, as a measure of peripheral sympathetic autonomic function, is altered by SCS. A second aim was to compare skin conductance levels of patients with failed back surgery syndrome (FBSS) with age- and sex-matched healthy controls. Twenty-three patients with FBSS treated with SCS participated in this study. Sudomotor function was measured with the SudoscanTM instrument on the hands and feet during SCS on and off states. Difference scores in skin conductance between patients and age- and sex-matched healthy controls were calculated. Normal sudomotor function at the painful lower limb was revealed for 61% of the patients when SCS was activated. Skin conductance levels were not altered between on and off states of SCS. Differences in scores between patients and healthy controls were significantly different from zero. This study showed that SCS does not influencing the sympathetic nervous system in patients with FBSS, as measured by skin conductance levels. Moreover, it suggested that there is no normalization of the functioning of the sympathetic nervous system, despite the effectiveness of SCS to reduce pain intensity.


1981 ◽  
Vol 240 (3) ◽  
pp. E314-E319 ◽  
Author(s):  
J. B. Young ◽  
L. Landsberg

Fasting decreases and cold exposure increases sympathetic nervous system activity. The present studies examine the effect of fasting and cold together on sympathoadrenal function. At 4 degrees C animals fasted for 2 days excreted 29% less norepinephrine (NE) than fed animals, averaging 458 +/- 32ng NE/mg creatinine and 646 +/- 68, respectively (P less than 0.005), but 122% more epinephrine (E) 77.9 +/- 11.7 ng E/mg creatinine and 35.1 +/- 6.7, respectively (P less than .01). Fasting for 2 days reduced cardiac NE turnover, a direct measure of sympathetic neuronal activity, 33% in animals at 22 degrees C from 28.2 +/- 3.6 ng NE . heart-1 . h-1 to 18.9 +/- 4.8 (95% confidence intervals) and 25% in animals acutely exposed to 4 degrees C from 60.7 +/- 8.0 to 45.6 +/- 9.5. Similar reductions in urinary NE excretion and cardiac NE turnover were observed in adrenal-demedullated rats. Thus fasting at 4 degrees C lowers sympathetic activity and enhances adrenal medullary secretion. This pattern of decreased sympathetic and increased adrenal medullary activity, previously seen with fasting hypoglycemia, suggests an important role for the adrenal medulla in internal homeostasis at times when the sympathetic nervous system is suppressed.


1992 ◽  
Vol 263 (4) ◽  
pp. F586-F593 ◽  
Author(s):  
P. A. Daly ◽  
J. B. Young ◽  
L. Landsberg

Renal sympathetic nervous system (SNS) responses to environmental temperature and diet were evaluated using [3H]norepinephrine ([3H]NE) turnover as the index of sympathetic activity. Pharmacological studies first demonstrated that renal NE was localized principally within storage granules of renal sympathetic nerves and regulated by central sympathetic outflow. Acute exposure to cold (4 degrees C), which increased cardiac SNS activity (P < 0.00005), had no effect on renal SNS. A 48-h fast suppressed renal [3H]NE turnover by 37% (P = 0.00024) and cardiac [3H]NE turnover by 48% (P = 0.00608). Dietary supplementation with sucrose did not affect [3H]NE turnover in kidney in either of two separate experiments, although it increased cardiac NE turnover in both. On the other hand, lard feeding significantly increased [3H]NE turnover in both kidney and heart, whereas dietary protein supplementation exerted no effect on either renal or cardiac [3H]NE turnover. These studies demonstrate a unique pattern of sympathetic regulation in kidney, one which is highly responsive to fasting and dietary fat, but not to cold exposure or dietary sucrose.


1987 ◽  
Vol 400 (1) ◽  
pp. 35-39 ◽  
Author(s):  
Marvin Brown ◽  
Roberta Allen ◽  
Laurel Fisher

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