Document Detail


Cardiac sympathetic afferent activation provoked by myocardial ischemia and reperfusion. Mechanisms and reflexes.
MedLine Citation:
PMID:  11458709     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cardiac sympathetic afferents are known to reflexly activate the cardiovascular system, leading to increases in blood pressure, heart rate, and myocardial contractile function. During myocardial ischemia, these sensory nerves also transmit the sensation of pain (angina pectoris) and cause tachyarrhythmias. The authors' laboratory has been interested in defining the mechanisms of activation of this neural system during ischemia and reperfusion. During these periods, reactive oxygen species, particularly hydroxyl radicals, are produced from the breakdown of purine metabolites and lead to stimulation of sympathetic (and vagal) ventricular chemosensitive nerve endings. For example, stimulation with hydrogen peroxide leads to a small reflex increase in blood pressure from the predominant sympathetic afferent activation that is reduced by simultaneous activation of cardiac vagal afferents (known to exert predominantly depressor reflexes). Central integration of these two opposing reflexes likely occurs at several regions of the brain stem, including the nucleus tractus solitarii, where neural occlusion occurs during simultaneous cardiac sympathetic and vagal-afferent stimulation. Activation of platelets also appears to play a role during myocardial ischemia, leading to local release of serotonin (5HT), which, through a 5HT3 mechanism, stimulates sympathetic afferents. Finally, regional changes in pH from lactic acid (but not hypercapnia), stimulate ventricular afferents and may activate kallikrein to increase bradykinin (BK), which, in turn, breaks down arachidonic acid to form prostaglandins. Prostaglandins sensitize cardiac sympathetic afferents to BK. Thus, stimulation of cardiac sympathetic afferents during ischemia and reperfusion and the resulting reflex events form a multifactorial process resulting from activation of a number of chemical pathways in the myocardium.
Authors:
J C Longhurst; S C Tjen-A-Looi; L W Fu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Annals of the New York Academy of Sciences     Volume:  940     ISSN:  0077-8923     ISO Abbreviation:  Ann. N. Y. Acad. Sci.     Publication Date:  2001 Jun 
Date Detail:
Created Date:  2001-07-18     Completed Date:  2001-08-09     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  7506858     Medline TA:  Ann N Y Acad Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  74-95     Citation Subset:  IM    
Affiliation:
Department of Medicine, Medical Sciences 1, C240, University of California at Irvine, Irvine, CA 92697, USA. jcl@uci.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Heart / innervation*
Myocardial Ischemia / physiopathology*
Myocardial Reperfusion Injury / physiopathology*
Neurons, Afferent / physiology*
Reflex / physiology
Sympathetic Nervous System / physiopathology*
Grant Support
ID/Acronym/Agency:
HL-36527/HL/NHLBI NIH HHS; HL-51428/HL/NHLBI NIH HHS

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


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