Whole body response of the peripheral circulation following hemorrhage in the rat

1979 ◽  
Vol 236 (2) ◽  
pp. H206-H210
Author(s):  
R. E. Samar ◽  
T. G. Coleman
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Driving Force ◽  
Venous Return ◽  
Peripheral Circulation ◽  
Filling Pressure ◽  
Whole Body ◽  
Untreated Animal ◽  
Sympathetic Nervous ◽  
Body Response

Changes in mean circulatory filling pressure (MCFP) after hemorrhage reflect the whole-body response of the peripheral circulation to restore the driving force for venous return. In this study, changes in MCFP were measured for 15 min following a rapid 8 ml/kg hemorrhage. Three groups of rats were studied: 1) conscious, untreated; 2) conscious, ganglion blocked; and 3) pentobarbital anesthetized. In all three groups, hemorrhage decreased MCFP approximately 2.6 mmHg immediately after hemorrhage. In the conscious untreated rat, MCFP recovered 1.3 mmHg in 15 min; 83% of this recovery was complete within 2 min, and over 50% was complete by 30 s posthemorrhage. With ganglionic blockade, recovery was slowed to about 70% of that in the conscious, untreated animal during the first 5 min after hemorrhage. MCFP recovery was substantially depressed by pentobarbital, averaging only 42% of that in the untreated animal 5 min after hemorrhage. The results demonstrate that peripheral changes can quickly restore nearly 50% of the MCFP decrease occurring immediately after mild hemorrhage and that about one-third of this response is mediated by the sympathetic nervous system. Pentobarbital anesthesia greatly inhibits recovery, although its repressive mechanism is not known.

scholarly journals OR04-02 The Role of the Sympathetic Nervous System in Metabolic Disorder and Adipose Dysfunction in Obesity and Aging

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Kenichi Sakamoto ◽  
Chunxue Zhou ◽  
Giulia Maurizi ◽  
Claudia Liberini ◽  
Ling Li ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Nervous System ◽  
Adipose Tissue ◽  
Sympathetic Nervous System ◽  
Fasting Blood Glucose ◽  
De Novo Lipogenesis ◽  
Whole Body ◽  
Peripheral Tissues ◽  
Sympathetic Nervous

Abstract Both obesity and aging increase susceptibility to metabolic disease and type 2 diabetes where adipose tissue dysfunction is a hallmark. In both conditions, impaired autonomic control is believed to play a key role in disrupted CNS control of metabolism. However, the role of the sympathetic nervous system (SNS) and catecholaminergic signaling in metabolic disease has not been well defined in large part due to a lack of suitable animal models(1). Surgical denervation is not specific to the SNS and chemical sympathectomy through 6-hydroxydopamine causes inflammation due to toxic effects. Abrogation of catecholamine (CA) synthesis in the whole body due to genetic deletion of the gene for tyrosine hydroxylase (th), a key enzyme in CA synthesis, results in embryonic lethality likely due to the lack of dopamine and norepinephrine in the CNS where they serve as key neurotransmitters. Here we studied the role of the SNS and catecholaminergic signaling in metabolic control in both aging as well as high fat diet (HFD) induced obesity. We created a mouse model of inducible th gene deletion that is restricted to the periphery, including sympathetic fibers of the peripheral NS but spares the brain as a pharmaco-genetic model of sympathectomy(2). TH is deleted and CA levels were reduced more than 90% in peripheral tissues of TH KO mice, while intact in the CNS. TH KO mice are cold intolerant consistent with functional sympathectomy. Interestingly, TH KO mice are protected from HFD feeding induced glucose intolerance (AUC during GTT: WT1018.8±42.0 mg/dl/hr vs. TH KO 485.0±85.8 mg/dl/hr; p < 0.0001; n = 6) even though food intake increased in TH KO mice. In 20 months old TH KO mice glucose tolerance was improved and fasting blood glucose levels were reduced (AUC during GTT: WT 357.3±16.2 mg/dl/hr vs. TH KO 254.5±15.6 mg/dl/hr; p < 0.01; n = 12) with higher insulin levels (WT 0.35±0.07 μg/l vs. TH KO 1.28±0.28 μg/l; p < 0.001; n = 9). Of note, insulin tolerance tests did not show marked differences. Both obesity and aging are characterized by impaired adipose tissue function with reduced lipogenic capacity. TH KO mice fed a HFD exhibit increased WAT de novo lipogenesis, lower lipolysis, and trend to exhibit decreased adipose tissue inflammation, suggesting that the SNS is a major culprit for the impaired lipogenic capacity in adipose tissue. Our data provides support for the paradigm that impaired SNS function plays an important role in the dysmetabolic states of obesity and aging. Reference 1. Ryu V, Buettner C. Fat cells gobbling up norepinephrine? PLoS Biol. 2019;17(2):e3000138. 2. Fischer K, Ruiz HH, Jhun K, Finan B, Oberlin DJ, van der Heide V, et al. Alternatively activated macrophages do not synthesize catecholamines or contribute to adipose tissue adaptive thermogenesis. Nature medicine. 2017;23(5):623-30.

Thyroid hormone-catecholamine interrelationships during exposure to cold

1981 ◽  
Vol 97 (1) ◽  
pp. 91-97 ◽  
Author(s):  
H. Storm ◽  
C. van Hardeveld ◽  
A. A. H. Kassenaar
Keyword(s):  
Nervous System ◽  
Plasma Concentration ◽  
Thyroid Hormone ◽  
Sympathetic Nervous System ◽  
Plasma Levels ◽  
Surgical Procedure ◽  
Exposure To Cold ◽  
Basal Plasma ◽  
Sympathetic Nervous

Abstract. Basal plasma levels for adrenalin (A), noradrenalin (NA), l-triiodothyronine (T3), and l-thyroxine (T4) were determined in rats with a chronically inserted catheter. The experiments described in this report were started 3 days after the surgical procedure when T3 and T4 levels had returned to normal. Basal levels for the catecholamines were reached already 4 h after the operation. The T3/T4 ratio in plasma was significantly increased after 3, 7, and 14 days in rats kept at 4°C and the same holds for the iodide in the 24-h urine after 7 and 14 days at 4°C. The venous NA plasma concentration was increased 6- to 12-fold during the same period of exposure to cold, whereas the A concentration remained at the basal level. During infusion of NA at 23°C the T3/T4 ratio in plasma was significantly increased after 7 days compared to pair-fed controls, and the same holds for the iodide excretion in the 24-h urine. This paper presents further evidence for a role of the sympathetic nervous system on T4 metabolism in rats at resting conditions.

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