| Intrinsic cardiac nervous system in tachycardia induced heart failure. | |
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MedLine Citation:
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PMID: 12893651 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Rakesh C Arora; Rene Cardinal; Frank M Smith; Jeffrey L Ardell; Louis J Dell'Italia; J Andrew Armour |
Publication Detail:
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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:
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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:
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Created Date: 2003-10-14 Completed Date: 2003-11-21 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 100901230 Medline TA: Am J Physiol Regul Integr Comp Physiol Country: United States |
Other Details:
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Languages: eng Pagination: R1212-23 Citation Subset: IM |
Affiliation:
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Centre de Recherche, Hôpital du Sacré-coeur, 5400 Boulevard Gouin ouest, Montréal, QC, Canada H4J 1C5. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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HL-58140/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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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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