Document Detail


Increased severity of reperfusion arrhythmias in mouse hearts lacking histamine H3-receptors.
MedLine Citation:
PMID:  12810089     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We had previously reported that activation of histamine H(3)-receptors (H(3)R) on cardiac adrenergic nerve terminals decreases norepinephrine (NE) overflow from ischemic hearts and alleviates reperfusion arrhythmias. Thus, we used transgenic mice lacking H(3)R (H(3)R(-/-)) to investigate whether ischemic arrhythmias might be more severe in H(3)R(-/-) hearts than in hearts with intact H(3)R (H(3)R(+/+)). We report a greater incidence and longer duration of ventricular fibrillation (VF) in H(3)R(-/-) hearts subjected to ischemia. VF duration was linearly correlated with NE overflow, suggesting a possible cause-effect relationship between magnitude of NE release and severity of reperfusion arrhythmias. Thus, our findings strengthen a protective antiarrhythmic role of H(3)R in myocardial ischemia. Since malignant tachyarrhythmias cause sudden death in ischemic heart disease, attenuation of NE release by selective H(3)R agonists may represent a new approach in the prevention and treatment of ischemic arrhythmias.
Authors:
Motohiro Koyama; Paul M Heerdt; Roberto Levi
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  306     ISSN:  0006-291X     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2003 Jul 
Date Detail:
Created Date:  2003-06-17     Completed Date:  2003-08-14     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  792-6     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY 10021, USA.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic alpha-Agonists / metabolism
Animals
Arrhythmias, Cardiac / metabolism*,  pathology
Electrocardiography
Female
Humans
Mice
Mice, Transgenic
Myocardial Ischemia
Myocardial Reperfusion Injury / metabolism*,  pathology
Norepinephrine / metabolism
Receptors, Histamine H3 / genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
HL34215/HL/NHLBI NIH HHS; HL46403/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Adrenergic alpha-Agonists; 0/Receptors, Histamine H3; 51-41-2/Norepinephrine

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


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