Document Detail


Intrinsic cardiac nervous system in tachycardia induced heart failure.
MedLine Citation:
PMID:  12893651     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The purpose of this study was to test the hypothesis that early-stage heart failure differentially affects the intrinsic cardiac nervous system's capacity to regulate cardiac function. After 2 wk of rapid ventricular pacing in nine anesthetized canines, cardiac and right atrial neuronal function were evaluated in situ in response to enhanced cardiac sensory inputs, stimulation of extracardiac autonomic efferent neuronal inputs, and close coronary arterial administration of neurochemicals that included nicotine. Right atrial neuronal intracellular electrophysiological properties were then evaluated in vitro in response to synaptic activation and nicotine. Intrinsic cardiac nicotine-sensitive, neuronally induced cardiac responses were also evaluated in eight sham-operated, unpaced animals. Two weeks of rapid ventricular pacing reduced the cardiac index by 54%. Intrinsic cardiac neurons of paced hearts maintained their cardiac mechano- and chemosensory transduction properties in vivo. They also responded normally to sympathetic and parasympathetic preganglionic efferent neuronal inputs, as well as to locally administered alpha-or beta-adrenergic agonists or angiotensin II. The dose of nicotine needed to modify intrinsic cardiac neurons was 50 times greater in failure compared with normal preparations. That dose failed to alter monitored cardiovascular indexes in failing preparations. Phasic and accommodating neurons identified in vitro displayed altered intracellular membrane properties compared with control, including decreased membrane resistance, indicative of reduced excitability. Early-stage heart failure differentially affects the intrinsic cardiac nervous system's capacity to regulate cardiodynamics. While maintaining its capacity to transduce cardiac mechano- and chemosensory inputs, as well as inputs from extracardiac autonomic efferent neurons, intrinsic cardiac nicotine-sensitive, local-circuit neurons differentially remodel such that their capacity to influence cardiodynamics becomes obtunded.
Authors:
Rakesh C Arora; Rene Cardinal; Frank M Smith; Jeffrey L Ardell; Louis J Dell'Italia; J Andrew Armour
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2003-07-31
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  285     ISSN:  0363-6119     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2003 Nov 
Date Detail:
Created Date:  2003-10-14     Completed Date:  2003-11-21     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R1212-23     Citation Subset:  IM    
Affiliation:
Centre de Recherche, Hôpital du Sacré-coeur, 5400 Boulevard Gouin ouest, Montréal, QC, Canada H4J 1C5.
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MeSH Terms
Descriptor/Qualifier:
Animals
Dogs
Female
Ganglia, Parasympathetic / cytology,  drug effects,  physiology
Heart / innervation*,  physiopathology*
Heart Failure / physiopathology*
Male
Membrane Potentials / drug effects
Neurons / drug effects,  physiology
Nicotine / pharmacology
Nicotinic Agonists / pharmacology
Pacemaker, Artificial
Physical Stimulation
Stimulation, Chemical
Sympathetic Nervous System / drug effects,  physiology
Tachycardia / physiopathology*
Veratridine / pharmacology
Grant Support
ID/Acronym/Agency:
HL-58140/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Nicotinic Agonists; 54-11-5/Nicotine; 71-62-5/Veratridine

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


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