Document Detail


Function and bioenergetics in isolated perfused trained rat hearts.
MedLine Citation:
PMID:  9038963     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To evaluate the resistance of physiologically hypertrophied hearts to hypoxic insult, we quantified the development of functional deficits during hypoxia and reoxygenation in hypertrophied hearts from swim-trained female rats and we correlated this with assessment of high-energy phosphate (HEP) metabolites from simultaneous 31P nuclear magnetic resonance (NMR) measurements. Furthermore, in vivo enzymatic studies were carried out with saturation transfer NMR under well-oxygenated perfusion conditions for both beating and KCl-arrested hearts. Finally, in vitro enzymatic assays were performed. During hypoxia, the trained hearts exhibited improved systolic and diastolic function compared with hearts from sedentary animals. After 16 min of hypoxia, left ventricular (LV) developed pressure fell to 9% of baseline in control hearts but to only 21% of baseline in trained hearts (P < 0.01). LV diastolic function was also improved by training, increasing during hypoxia from a baseline of 10 to 71.0 +/- 3.3 mmHg in control hearts and to 55.3 +/- 4.8 mmHg in trained hearts (P < 0.05). Trained hearts also showed more rapid and complete recovery of function during reoxygenation and greater coronary flow per gram of heart throughout the entire protocol. Functional differences were not accompanied by differences in HEP at baseline; moreover, ATP and phosphocreatine (PCr) loss during hypoxia was similar between control and trained hearts, as was the recovery of PCr during reoxygenation. Saturation transfer experiments showed an increase in the forward creatine kinase (CrK) rate constant in trained hearts of 18% while beating, whereas in vitro enzymatic analysis revealed a 16% increase in the ratio of mitochondrial CrK to citrate synthase activity in LV tissue. Thus the relative preservation of function in hearts from trained rats could not be accounted for by overall HEP levels but may reflect adaptations in the CrK system.
Authors:
R G Spencer; P M Buttrick; J S Ingwall
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  272     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1997 Jan 
Date Detail:
Created Date:  1997-03-31     Completed Date:  1997-03-31     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H409-17     Citation Subset:  IM; S    
Affiliation:
National Institutes of Health, National Institute on Aging, Baltimore, Maryland 21224, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism
Animals
Anoxia / physiopathology
Creatine Kinase / metabolism
Energy Metabolism*
Female
Heart / anatomy & histology,  drug effects,  physiology*
Magnetic Resonance Spectroscopy
Muscle, Skeletal / metabolism
Myocardium / metabolism*
Organ Size
Oxygen / pharmacology
Oxygen Consumption
Perfusion
Phosphocreatine / metabolism
Physical Conditioning, Animal*
Rats
Rats, Wistar
Grant Support
ID/Acronym/Agency:
HL-15498/HL/NHLBI NIH HHS; HL-43170/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
56-65-5/Adenosine Triphosphate; 67-07-2/Phosphocreatine; 7782-44-7/Oxygen; EC 2.7.3.2/Creatine Kinase

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


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