Haemodynamic Responses to Exercise in Hypertension: Place of the Sympathetic Nervous System Evaluated by a New Selective Cardiac Beta-adrenergic Blocking Agent ICI 50,172

1968 ◽  
Vol 2 (4) ◽  
pp. 379-383 ◽  
Author(s):  
E. Shinebourne ◽  
J. Fleming ◽  
J. Hamer
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Blocking Agent ◽  
Beta Adrenergic ◽  
Sympathetic Nervous ◽  
Adrenergic Blocking

Role of the sympathetic nervous system in CCl4 hepatotoxicity

1960 ◽  
Vol 198 (3) ◽  
pp. 669-676 ◽  
Author(s):  
Deane N. Calvert ◽  
Theodore M. Brody
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Liver Mitochondria ◽  
Central Vein ◽  
Fat Depots ◽  
Sympathetic Nervous ◽  
Adrenergic Blocking ◽  
Stimulation Of

An hypothesis is proposed which states that the characteristic hepatic changes seen after the administration of carbon tetrachloride are the result of stimulation of central sympathetic areas which produce a massive discharge of the peripheral sympathetic nervous system. Stimulation of the sympathetic supply to the blood vessels of the liver results in restriction of blood flow in the liver, leading to anoxia and the characteristic necrosis around the central vein of the hepatic lobule. Similarly the discharge causes the release of unesterified fatty acids from the peripheral fat depots and the consequent deposition of lipid in the liver. This hypothesis is based upon experimental evidence using the following physiologic and pharmacologic maneuvers: adrenergic blocking agents, pretreatment with reserpine, adrenalectomy and section of the spinal cord—all are effective to a greater or lesser extent in preventing the changes characteristically seen in oxidative phosphorylation of the liver mitochondria, activation of a Mg-dependent ATPase and deposition of lipid in the liver. Transection of the spinal cord is the most effective treatment and prevents entirely the characteristic changes seen in the above-mentioned functions.

Lack of Influence of the Sympathetic Nervous System on the Calorigenic Response to Thyroxine

1957 ◽  
Vol 188 (3) ◽  
pp. 503-506 ◽  
Author(s):  
A. Surtshin ◽  
James K. Cordonnier ◽  
S. Lang
Keyword(s):  
Nervous System ◽  
Oxygen Consumption ◽  
Sympathetic Nervous System ◽  
Significant Rise ◽  
Published Data ◽  
Physiological Effects ◽  
Concurrent Administration ◽  
Rate Of Oxygen Consumption ◽  
Sympathetic Nervous ◽  
Adrenergic Blocking

Normal rats as well as thyroparathyroidectomized rats concurrently given thyroxine and an adrenergic blocking dose of Dibenzyline show the expected rise in rate of oxygen consumption. After bilateral adrenal demedullation the resting rate of oxygen consumption is not significantly different from normal, and injection of a large dose of thyroxine either with or without concurrent administration of adrenergic blocking doses of Dibenzyline is followed by a significant rise in the rate of oxygen consumption. Our data and other pertinent published data lend support neither to the claim that the calorigenic effect of exogenous thyroxine is dependent upon the presence of normally acting adrenal medullary hormones nor to the claim that the metabolic changes of thyrotoxicosis are due to the physiological effects of epinephrine and norepinephrine as augmented by the thyroid hormones.

Ontogeny of canine intrathoracic cardiac nervous system

1991 ◽  
Vol 261 (4) ◽  
pp. R920-R927 ◽  
Author(s):  
C. Haddad ◽  
J. A. Armour
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Adrenergic Receptors ◽  
Beta Agonist ◽  
Canine Heart ◽  
Cardiac Innervation ◽  
Beta Adrenergic Receptors ◽  
Parasympathetic Innervation ◽  
Beta Adrenergic ◽  
Sympathetic Nervous

The functional cardiac innervation of 61 puppies from nine different litters (2-8 littermates), ranging in age from 1 day to 7 wk, was investigated. The efferent sympathetic nervous system exerted minimal effects on the heart of 1-day-old puppies, gradually influencing the heart more thereafter such that by 7 wk of life it was functionally mature. In contrast, efferent parasympathetic cardiac innervation was well developed at birth, maturing thereafter such that by 4-7 wk of age its capacity to modulate the heart was similar to that found in adults. The right- and left-sided efferent sympathetic and parasympathetic intrathoracic nervous systems induced similar cardiac modulation throughout this period of development. Cardiac myocyte beta-adrenergic receptors were partially functional at birth, as determined by responses elicited by supramaximal doses of the beta-agonist isoproterenol. Responses elicited by isoproterenol became greater over the following 7 wk of life, when they were found to be similar to those elicited in adults. By 1 wk of age, synaptic mechanisms in intrathoracic sympathetic ganglia involved in cardiac regulation were relatively well developed, with cardiopulmonary-cardiac reflexes present but not functionally mature at that age. It is concluded that maturation of the efferent sympathetic nervous system modulating the canine heart depends to a large extent on the ontogeny of cardiac beta-adrenergic receptors rather than the ontogeny of synapses in intrathoracic ganglia. Furthermore, even though functional cardiac efferent parasympathetic innervation is present before efferent sympathetic innervation, both reach maturity at about the same age.

BETA-ADRENERGIC MEDIATION OF SYMPATHETIC NERVOUS SYSTEM ACTIVITY

1982 ◽  
Vol 10 (3) ◽  
pp. 221
Author(s):  
Bart Chernow ◽  
Michael Ziegler ◽  
Joseph Coyle ◽  
David Cruess ◽  
Pat Hughes ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nervous System Activity ◽  
Beta Adrenergic ◽  
System Activity ◽  
Nervous System Activity ◽  
Sympathetic Nervous

scholarly journals Indirect autonomic nervous system activity assessment in patients with myocardial infarction

2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
VA Aleksandrenko ◽  
EA Kuzheleva ◽  
AA Garganeeva
Keyword(s):  
Myocardial Infarction ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Sympathetic Nervous System ◽  
Autonomic Nervous System Activity ◽  
Beta Adrenergic ◽  
System Activity ◽  
Autonomic Nervous ◽  
Nervous System Activity ◽  
Sympathetic Nervous

Abstract Funding Acknowledgements Type of funding sources: None. Introduction. Abnormalities in the cardiac sympathetic nervous system have been documented in myocardial infarction (MI) and have been directly implicated in pathogenesis and progression of MI. Assessment of the autonomic nervous system activity in acute stage of MI allowed us to identify groups of high-risk patients. Purpose. To investigate the sympathetic nervous system activity in patients with MI by assessing the condition of beta-adrenergic reactivity of erythrocytes. To analyze ADRB1 Arg389Gly associations with the state of beta-adrenergic reactivity of erythrocytes in patients with MI. Methods. During the study period, 62 patients were enrolled. The patients were divided into 2 groups. The first group consisted of 11 patients (nine women and two men, median age of 54.0 [49.0;61.0] years) with normal beta-adrenergic reactivity of erythrocytes, the second group consisted of 51 patients (40 women and 11 man, median age of 61.0 [48.0;72.0] years) with abnormal beta-adrenergic reactivity of  erythrocytes. The research of beta-adrenergic reactivity of erythrocytes was conducted by analysis of changing erythrocyte osmoresistance under the influence of beta blocker in the first 6 hours from the onset of the heart attack. The genetic research was conducted by PСR method in real time. Results. Groups of patients were comparable in main clinical indicators (anamnesis of ischemic heart disease and chronic heart failure, frequency of beta blockers administration before and during of MI, electrocardiography features: elevation of ST-segment, Q-wave and etc.). The second group presented with a higher occurrence of acute left ventricular failure (33.3% vs 0%, p = 0.026) and arterial hypertension (90.2% vs 63.6%, p = 0.044). Parameters of myocardial damage were significantly higher in the second group than the first group. Primarily, this manifested in the presence of a greater number of hypokinesis zones on echocardiography (p = 0.015). In addition, patients of the second group had a lower ejection fraction according to echocardiography (51.0 [46.5;59.0]% vs 58.0 [52.0;63.0]%, p = 0.042). Levels of blood necrosis biomarkers were significantly higher in the second group, e.g. Troponin I (24.1 [9.9;68.0] ng/ml vs 1.3 [0.2;1.8] ng/ml, p = 0.001). At the same time statistically significant distinctions of the severity of coronary atherosclerosis in groups were not revealed. The analysis of ADRB1 Arg389Gly demonstrated association of CC-genotype with abnormal beta-adrenergic reactivity of erythrocytes [OR 5.9, 95% СI 1.16-30.25, p = 0.043]. Conclusion. Patients with an abnormal beta-adrenergic reactivity were characterized by a greater volume of damage to the heart muscle. Moreover, association of CC-genotype of gene ADRB1 Arg389Gly with abnormal beta-adrenergic reactivity of erythrocytes was identified.

Sympathectomy and beta-adrenergic blockade during lung maturation stimulated by TRH and cortisol in fetal sheep

1993 ◽  
Vol 75 (1) ◽  
pp. 141-147 ◽  
Author(s):  
J. C. Schellenberg ◽  
G. C. Liggins ◽  
J. A. Kitterman ◽  
C. C. Lee
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Adrenergic Blockade ◽  
Lung Maturation ◽  
Fetal Sheep ◽  
Beta Adrenergic ◽  
Adrenergic Mechanisms ◽  
Adrenergic Blocker ◽  
Sympathetic Nervous ◽  
6 Hydroxydopamine

To test whether beta-adrenergic mechanisms and the sympathetic nervous system are involved in the synergistic action of thyrotropin-releasing hormone (TRH) and cortisol on lung maturation, fetal sheep (n = 32) were infused from 121 to 128 days of gestation with saline, TRH + cortisol, TRH + cortisol + beta-adrenergic blocker, or TRH + cortisol after chemical sympathectomy with 6-hydroxydopamine. TRH + cortisol increased lung distensibility and stability and alveolar concentrations of saturated phosphatidylcholine two- to threefold over control fetuses. beta-Adrenergic blockade prevented the increase in distensibility in response to TRH + cortisol. Sympathectomy did not impair the increase in distensibility and stability in response to TRH + cortisol but inhibited the increase in alveolar total phospholipids. Tissue concentrations of saturated phosphatidylcholine increased in TRH + cortisol-treated fetuses after either sympathectomy or beta-adrenergic blockade. We concluded that during lung maturation by TRH + cortisol 1) sympathetic mechanisms are requisite for surfactant release, 2) nonneurogenic beta-adrenergic mechanisms are requisite for the maturation of the mechanical properties of the lung and 3) stimulation of surfactant synthesis is independent of beta-adrenergic action and the sympathetic nervous system.

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