Document Detail

Reversal of dysfunction in postischemic stunned myocardium by epinephrine and postextrasystolic potentiation.
MedLine Citation:
PMID:  3950238     Owner:  NLM     Status:  MEDLINE    
After brief coronary occlusions, myocardium may become "stunned," exhibiting prolonged depression of function despite the absence of necrosis. Because of the accompanying decline in adenosine triphosphate and adenine nucleotide precursors, a deficiency of energy supply has been proposed as the basis for postischemic dysfunction. This study examined whether sufficient functional and metabolic reserve exists in stunned myocardium to sustain a prolonged, maximal inotropic response to epinephrine and postextrasystolic potentiation. In 11 open chest dogs, the left anterior descending coronary artery was occluded for 5 minutes, followed by 10 minutes of reflow, repeated 12 times, with a final 1 hour recovery period. Regional myocardial function was measured using pairs of ultrasonic dimension crystals implanted in ischemic and nonischemic zones. During repetitive reflows a progressive decrease in mean systolic segment shortening occurred: baseline 21.8%, 1st reflow 15.2%, 12th reflow 4.3%, 1 hour recovery 7.9%. Intravenous epinephrine, titrated to produce a maximal inotropic response, caused segment shortening to increase to 21.6% after 10 minutes and to 24.8% after 1 hour of infusion, despite a 20 mm Hg increase in systolic pressure. The same dose of epinephrine given before ischemia increased segment shortening to 30.5%. In six of the dogs, postextrasystolic potentiation before ischemia increased segment shortening from 21.8 to 31.1%, and after 1 hour of recovery from ischemia, from 7.9 to 24.8%. Lesser increases in segment shortening were also seen in nonischemic segments. The results indicate that stunned myocardium possesses considerable functional reserve. Deficient energy stores are therefore not likely to be the basis for depressed function seen at rest in stunned myocardium.
L C Becker; J H Levine; A F DiPaula; T Guarnieri; T Aversano
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  7     ISSN:  0735-1097     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  1986 Mar 
Date Detail:
Created Date:  1986-03-31     Completed Date:  1986-03-31     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  580-9     Citation Subset:  AIM; IM    
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MeSH Terms
Arterial Occlusive Diseases / drug therapy*,  physiopathology,  therapy
Blood Pressure / drug effects
Cardiac Pacing, Artificial*
Coronary Disease / drug therapy*,  physiopathology,  therapy
Electric Stimulation
Epinephrine / pharmacology*
Myocardial Contraction / drug effects*
Myocardium / pathology
Regional Blood Flow
Systole / drug effects*
Time Factors
Grant Support
Reg. No./Substance:

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