Document Detail


Hemodynamics and mitochondrial energy metabolism in right heart hypertrophy after acute hypoxic stress.
MedLine Citation:
PMID:  10219464     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Excessive right heart hypertrophy was investigated under additional acute hypoxic stress to find out a possible contribution of mitochondrial dysfunction to sudden heart failure. Severe right heart hypertrophy in rats was induced by exposure to hypobaric pressure (46,663 Pa) for 4 weeks. Heart rate, isovolumic pressure and coronary flow were determined in the Langendorff mode of perfusion. After normoxia, the hearts were subdued to acute hypoxia/reoxygenation. Mitochondrial membrane potential was measured at the heart surface by fluorometry using 2-(dimethylaminostyryl)-l-ethylpyridinium iodide (DASPEI). At the end of each experiment mitochondria were isolated and ATP synthesis, ATPase, as well as creatine kinase activity were determined. Compared to normal hearts the heart rate is decreased in the hypertrophied group whereas right ventricular systolic and (end)diastolic pressure (adjusted to isovolumetric maxima) are increased. Coronary flow is decreased. Cytosolic creatine phosphate ATP levels and ATP/ADP ratios are significantly (p < 0.01) decreased. Furthermore, ATP synthesis and creatine kinase activities are diminished. At high ADP, respiration is loosely coupled or partially uncoupled. Acute hypoxia is particularly deleterious to hypertrophied hearts: Mitochondrial membrane potential as measured by heart surface fluorometry decreases extensively and is only very incompletely restored during reoxygenation. Rate-pressure product decreases precipitously and is restored during reoxygenation only to a very low extent. The results indicate an insufficient energy metabolism of mitochondria during acute hypoxia/reoxygenation which adds to the earlier described shifted isozyme pattern of myosin and decreased activities of myosin and sarcoreticular Ca2+ ATPase, leading to myocardial failure in right heart hypertrophy.
Authors:
T Thürich; J Bereiter-Hahn; M Schneider; G Zimmer
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Arzneimittel-Forschung     Volume:  49     ISSN:  0004-4172     ISO Abbreviation:  Arzneimittelforschung     Publication Date:  1999 Mar 
Date Detail:
Created Date:  1999-06-07     Completed Date:  1999-06-07     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0372660     Medline TA:  Arzneimittelforschung     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  212-20     Citation Subset:  IM    
Affiliation:
Zentrum der Inneren Medizin, Johann Wolfgang Goethe-Universität, Frankfurt, Germany.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphatases / metabolism
Adenosine Triphosphate / biosynthesis
Animals
Anoxia / enzymology,  metabolism*,  physiopathology*
Blood Pressure / drug effects
Creatine Kinase / metabolism
Cytosol / metabolism
Electrocardiography / drug effects
Energy Metabolism / physiology*
Hemodynamics / physiology*
Hypertrophy, Right Ventricular / enzymology,  metabolism*,  physiopathology*
Male
Membranes / metabolism
Mitochondria, Heart / enzymology,  metabolism*
Perfusion
Phosphates / metabolism
Rats
Rats, Wistar
Stress, Physiological / metabolism,  physiopathology
Chemical
Reg. No./Substance:
0/Phosphates; 56-65-5/Adenosine Triphosphate; EC 2.7.3.2/Creatine Kinase; EC 3.6.1.-/Adenosine Triphosphatases

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


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