Document Detail

Dynamic interaction between the heart and its sympathetic innervation following T5 spinal cord transection.
MedLine Citation:
PMID:  22723636     Owner:  NLM     Status:  MEDLINE    
Midthoracic spinal cord injury (SCI) is associated with enhanced sympathetic support of heart rate as well as myocardial damage related to calcium overload. The myocardial damage may elicit an enhanced sympathetic support of contractility to maintain ventricular function. In contrast, the level of inotropic drive may be reduced to match the lower afterload that results from the injury-induced reduction in arterial pressure. Accordingly, the inotropic response to midthoracic SCI may be increased or decreased but has not been investigated and therefore remains unknown. Furthermore, the altered ventricular function may be associated with anatomical changes in cardiac sympathetic innervation. To determine the inotropic drive following midthoracic SCI, a telemetry device was used for repeated measurements of left ventricular (LV) function, with and without beta-adrenergic receptor blockade, in rats before and after midthoracic SCI or sham SCI. In addition, NGF content (ELISA) and dendritic arborization (cholera toxin B immunohistochemistry and Sholl analysis) of cardiac-projecting sympathetic postganglionic neurons in the stellate ganglia were determined. Midthoracic SCI was associated with an enhanced sympathetic support of heart rate, dP/dt(+), and dP/dt(-). Importantly, cardiac function was lower following blockade of the sympathetic nervous system in rats with midthoracic SCI compared with sham-operated rats. Finally, these functional neuroplastic changes were associated with an increased NGF content and structural neuroplasticity within the stellate ganglia. Results document impaired LV function with codirectional changes in chronotropic and inotropic responses following midthoracic SCI. These functional changes were associated with a dynamic interaction between the heart and its sympathetic innervation.
Heidi L Lujan; Hussein Janbaih; Stephen E DiCarlo
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-06-21
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  113     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-16     Completed Date:  2013-06-17     Revised Date:  2013-10-17    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1332-41     Citation Subset:  IM    
Department of Physiology, Wayne State University School of Medicine, 540 E. Canfield Ave., Detroit, MI 48201, USA.
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MeSH Terms
Adrenergic beta-Antagonists / pharmacology
Arterial Pressure / drug effects,  physiology
Dendrites / drug effects,  metabolism,  physiology
Heart / drug effects,  innervation*,  physiopathology*
Heart Rate / drug effects,  physiology
Myocardium / metabolism
Nerve Growth Factor / metabolism
Neuronal Plasticity / drug effects,  physiology
Neurons / drug effects,  metabolism,  physiology
Rats, Sprague-Dawley
Receptors, Adrenergic, beta / metabolism
Spinal Cord Injuries / metabolism,  physiopathology*
Stellate Ganglion / drug effects,  metabolism,  physiopathology
Sympathetic Nervous System / drug effects,  metabolism,  physiopathology*
Ventricular Function, Left / drug effects,  physiology
Grant Support
Reg. No./Substance:
0/Adrenergic beta-Antagonists; 0/Receptors, Adrenergic, beta; 9061-61-4/Nerve Growth Factor

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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