Differential control of sympathetic outflow

2001 ◽  
Vol 281 (3) ◽  
pp. R683-R698 ◽  
Author(s):  
Shaun F. Morrison

With advances in experimental techniques, the early views of the sympathetic nervous system as a monolithic effector activated globally in situations requiring a rapid and aggressive response to life-threatening danger have been eclipsed by an organizational model featuring an extensive array of functionally specific output channels that can be simultaneously activated or inhibited in combinations that result in the patterns of autonomic activity supporting behavior and mediating homeostatic reflexes. With this perspective, the defense response is but one of the many activational states of the central autonomic network. This review summarizes evidence for the existence of tissue-specific sympathetic output pathways, which are likely to include distinct populations of premotor neurons whose target specificity could be assessed using the functional fingerprints developed from characterizations of postganglionic efferents to known targets. The differential responses in sympathetic outflows to stimulation of reflex inputs suggest that the circuits regulating the activity of sympathetic premotor neurons must have parallel access to groups of premotor neurons controlling different functions but that these connections vary in their ability to influence different sympathetic outputs. Understanding the structural and physiological substrates antecedent to premotor neurons that mediate the differential control of sympathetic outflows, including those to noncardiovascular targets, represents a challenge to our current technical and analytic approaches.

2011 ◽  
Vol 300 (5) ◽  
pp. R1230-R1240 ◽  
Author(s):  
Patrick J. Mueller ◽  
Nicholas A. Mischel ◽  
Tadeusz J. Scislo

Under acute and chronic conditions, the sympathetic nervous system can be activated in a differential and even selective manner. Activation of the rostral ventrolateral medulla (RVLM) has been implicated in differential control of sympathetic outputs based on evidence primarily in the cat. Although several studies indicate that differential control of sympathetic outflow occurs in other species, only a few studies have addressed whether the RVLM is capable of producing varying patterns of sympathetic activation in the rat. Therefore, the purpose of the present study was to determine whether activation of the RVLM results in simultaneous and differential increases in preganglionic adrenal (pre-ASNA), renal (RSNA), and lumbar (LSNA) sympathetic nerve activities. In urethane-chloralose anesthetized rats, pre-ASNA, RSNA, and LSNA were recorded simultaneously in all animals. Microinjections of selected concentrations and volumes of glutamate increased pre-ASNA, RSNA, and LSNA concurrently and differentially. Pre-ASNA and RSNA (in most cases) exhibited greater increases compared with LSNA on a percentage basis. By varying the volume or location of the glutamate microinjections, we also identified individual examples of differential and selective activation of these nerves. Decreases in arterial pressure or bilateral blockade of RVLM GABAA receptors also revealed differential activation, with the latter having a 3- to 4-fold greater effect on sympathetic activity. Our data provide evidence that activation of the rat RVLM increases renal, lumbar, and preganglionic adrenal sympathetic nerve activities concurrently, differentially, and, in some cases, selectively.


2016 ◽  
Vol 5 (03) ◽  
pp. 4882
Author(s):  
Vineeta Pande ◽  
Agarkhedkar S. R. ◽  
Ayank Tandon* ◽  
Aditya Agarwal

HLH is an uncommon, life threatening clinical syndrome cause by a severe hyper inflammatory reaction triggered by an infectious agent. The characteristic symptoms of HLH are due to the persistent stimulation of lymphocytes and histiocytes, leading to hyper-cytokinemia. We report a case of HLH in enteric fever in a13 year old female presenting with fever, lymphadenopathy and pancytopenia due an infection caused by Salmonella.


2017 ◽  
Vol 55 (8) ◽  
pp. 1112-1114 ◽  
Author(s):  
Giuseppe Lippi ◽  
Gianfranco Cervellin ◽  
Mario Plebani

AbstractThe management of laboratory data in unsuitable (hemolyzed) samples remains an almost unresolved dilemma. Whether or not laboratory test results obtained by measuring unsuitable specimens should be made available to the clinicians has been the matter of fierce debates over the past decades. Recently, an intriguing alternative to suppressing test results and recollecting the specimen has been put forward, entailing the definition and implementation of specific algorithms that would finally allow reporting a preanalytically altered laboratory value within a specific comment about its uncertainty of measurement. This approach carries some advantages, namely the timely communication of potentially life-threatening laboratory values, but also some drawbacks. These especially include the challenging definition of validated performance specifications for hemolyzed samples, the need to producing reliable data with the lowest possible uncertainty, the short turnaround time for repeating most laboratory tests, the risk that the comments may be overlooked in short-stay and frequently overcrowded units (e.g. the emergency department), as well as the many clinical advantages of a direct communication with the physician in charge of the patient. Despite the debate remains open, we continue supporting the suggestion that suppressing data in unsuitable (hemolyzed) samples and promptly notifying the clinicians about the need to recollect the samples remains the most (clinically and analytically) safe practice.


1960 ◽  
Vol 198 (3) ◽  
pp. 669-676 ◽  
Author(s):  
Deane N. Calvert ◽  
Theodore M. Brody

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.


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