Document Detail


Hyperlipidemia with hypoglycemia reduces myocardial oxygen utilization efficiency but not contractile function during coronary hypoperfusion.
MedLine Citation:
PMID:  10900179     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study was designed to determine changes in myocardial contractile function and fuel selection during moderate coronary hypoperfusion in the presence of elevated plasma free fatty acid (FFA) at normal and reduced blood glucose concentrations. Coronary perfusion pressure (CPP) was sequentially lowered from 100 to 60, 50, and 40 mmHg in the left anterior descending coronary artery (LAD) of anesthetized, open-chest dogs. Regional glucose uptake (GU), fatty acid uptake (FAU), percentage segment shortening (%SS), and oxygen consumption (MV O(2)) were determined with normal arterial plasma FFA concentrations (Group 1) or with elevated FFA concentrations (Groups 2 and 3). In Group 3, glucose in the coronary perfusate blood was reduced from 3.53+/-0.36 to 0.15+/-0.03 m M by hemodialysis. In Group 1, FAU fell by 85% as CPP was lowered to 60 mmHg and remained depressed as CPP was reduced further; GU did not fall significantly. Hyperlipidemia in Group 2 did not alter GU at any CPP, but maintained FAU at baseline levels until CPP was lowered to 40 mmHg. At 40 mmHg CPP, myocardial function and metabolic variables were similar in Groups 1 and 2. In Group 3 at 40 mmHg, FAU increased four-fold and MV O(2)doubled v Groups 1 and 2, and GU fell to zero. Despite these metabolic changes, %SS in Group 3 was unchanged relative to Group 2. Addition of glucose to the dialysate prevented the effects of dialysis on FAU, GU, and MV O(2). Thus, preferential glucose oxidation sustains myocardial oxygen utilization efficiency [(heart rate x %SS x maximum left ventricular pressure)/MV O(2)] during hypoperfusion. Blocking preferential glucose oxidation by combined hyperlipidemia and hypoglycemia lowers oxygen utilization efficiency, but does not compromise myocardial contractile function.
Authors:
B J Hart; X Bian; R T Mallet; H F Downey
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  32     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2000 Aug 
Date Detail:
Created Date:  2000-10-06     Completed Date:  2000-10-06     Revised Date:  2011-03-09    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  1539-52     Citation Subset:  IM    
Copyright Information:
Copyright 2000 Academic Press.
Affiliation:
Department of Integrative Physiology, University of North Texas Health Science Center at Fort Worth, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107-2699, USA. bhart@hsc.unt.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Glucose / metabolism
Dogs
Fatty Acids / blood
Female
Glucose / metabolism
Glycogen / blood
Hemodynamics
Hyperlipidemias / metabolism*
Hypoglycemia / metabolism*
Ischemia
Lactic Acid / blood
Male
Myocardial Contraction / physiology*
Myocardium / metabolism*
Oxygen / blood,  metabolism*
Oxygen Consumption
Perfusion
Pressure
Grant Support
ID/Acronym/Agency:
HL35027/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Fatty Acids; 50-21-5/Lactic Acid; 50-99-7/Glucose; 7782-44-7/Oxygen; 9005-79-2/Glycogen

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


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