Document Detail


Reduction of sympathetic inotropic response after ischemia in dogs. Contributor to stunned myocardium.
MedLine Citation:
PMID:  3998147     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Eight open chest dogs underwent 25 min of coronary occlusion to determine whether brief myocardial ischemia disrupts the normal myocardial inotropic response to sympathetic nervous stimulation. If so, this could represent a mechanism contributing to postischemic myocardial dysfunction. Myocardial segment shortening was measured using ultrasonic dimension crystals before and after coronary artery occlusion and reperfusion. Left ansa subclavia stimulation and systemic norepinephrine (NE) infusion were used to test the myocardial inotropic response to neural stimulation and direct exposure to the sympathetic mediator, respectively. Before coronary artery occlusion, base-line preischemic segment shortening (12.5 +/- 1.6%) (SEM) increased during both sympathetic stimulation (20.2 +/- 1.4%) and NE infusion (19.7 +/- 1.1%). The control segment responded similarly. After ischemia and reperfusion there was no significant change in heart rate, aortic or left ventricular pressures, nor changes in control segment shortening. In contrast, shortening in the postischemic segment was markedly reduced compared to baseline (4.1 +/- 2.4%), and no longer responded to sympathetic stimulation (2.4 +/- 2.8%), while responsiveness to systemic NE was maintained (12.9 +/- 2.0%), P less than 0.001, which suggested injury to the sympathetic-neural axis during the period of ischemia. This reduced response to neural stimulation was persistent for up to 2 h after reperfusion. Left atrial or intracoronary infusion of bretylium tosylate, which releases norepinephrine from nerve terminals, resulted in an immediate inotropic response in the postischemic segment, which indicated that total depletion of NE from nerve terminals during the ischemic period had not occurred. Disruption of sympathetic neural responsiveness is likely a component of the mechanism of postischemic myocardial dysfunction whenever there is appreciable sympathetic drive to the heart.
Authors:
A A Ciuffo; P Ouyang; L C Becker; L Levin; M L Weisfeldt
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  75     ISSN:  0021-9738     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  1985 May 
Date Detail:
Created Date:  1985-07-03     Completed Date:  1985-07-03     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1504-9     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Bretylium Tosylate / pharmacology
Coronary Disease / physiopathology*
Dogs
Female
Hemodynamics / drug effects
Male
Myocardial Contraction* / drug effects
Myocardium / pathology*
Norepinephrine / pharmacology
Regional Blood Flow / drug effects
Sympathetic Nervous System / physiopathology*
Grant Support
ID/Acronym/Agency:
17655-7//PHS HHS
Chemical
Reg. No./Substance:
51-41-2/Norepinephrine; 61-75-6/Bretylium Tosylate
Comments/Corrections

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