Document Detail

Biochemical and morphological changes in myocardium during coronary occlusion and reperfusion in canine hearts: effects of propranolol on myocardial damage.
MedLine Citation:
PMID:  2611809     Owner:  NLM     Status:  MEDLINE    
To clarify the mechanism of irreversible myocardial damage, we studied the relationship between ischaemic mitochondrial dysfunction and leakage of lysosomal enzymes, and the effects of propranolol on myocardial damage. Open chest anaesthetised dogs were divided into six groups: 30 min occlusion of the left anterior coronary artery (LAD); 2 h LAD occlusion; 2 h LAD occlusion after premedication with 0.3 propranolol; 30 min LAD occlusion/l h reperfusion; 2 h LAD occlusion/l h reperfusion; and 2 h LAD occlusion/l h reperfusion after propranolol premedication. After occlusion or reperfusion, heart mitochondria were prepared from normal and occluded or reperfused areas, and mitochondrial function (rate of oxygen consumption in State III, and respiratory control index) was measured polarographically. Myocardial tissue was fractionated and activities of lysosomal enzymes (N-acetyl-beta-glucosaminidase and beta-glucuronidase) were measured. Electron microscopic studies were performed. Thirty min occlusion induced mitochondrial dysfunction without leakage of lysosomal enzymes. Reperfusion for 1 h reversed these changes. However occlusion for 2 h induced mitochondrial dysfunction associated with the leakage of lysosomal enzymes, and mitochondrial dysfunction was not reversed by 1 h reperfusion. Propranolol reduced mitochondrial dysfunction after 2 h occlusion and prevented leakage of lysosomal enzymes. Mitochondrial function was fairly well maintained after 1 h reperfusion in dogs premedicated with propranolol. Structural changes in mitochondria were observed in the 2 h occlusion/l h reperfusion group, and were reduced by premedication with propranolol. These results suggest that irreversible injury of ischaemic mitochondria is closely linked with instability of lysosomal membranes, and that propranolol prevented irreversible myocardial mitochondrial dysfunction.
T Ogawa; S Sugiyama; N Hieda; T Ito; T Satake; T Ozawa
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Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  Cardiovascular research     Volume:  23     ISSN:  0008-6363     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  1989 May 
Date Detail:
Created Date:  1990-03-06     Completed Date:  1990-03-06     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  417-23     Citation Subset:  IM    
Department of Internal Medicine, Faculty of Medicine, University of Nagoya, Japan.
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MeSH Terms
Heart / drug effects*
Intracellular Membranes / drug effects,  ultrastructure
Lysosomes / drug effects,  enzymology,  ultrastructure
Mitochondria, Heart / drug effects,  metabolism,  ultrastructure
Myocardial Infarction / drug therapy,  metabolism*,  pathology
Myocardial Reperfusion
Myocardium / metabolism*,  ultrastructure
Propranolol / pharmacology*,  therapeutic use
Time Factors
Reg. No./Substance:

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