Accelerated glycolysis and greater postischemic dysfunction in hypertrophied rat hearts are independent of coronary flow.

Accelerated glycolysis and greater postischemic dysfunction in hypertrophied rat hearts are independent of coronary flow. Research Abstract Details 

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Accelerated glycolysis and greater postischemic dysfunction in hypertrophied rat hearts are independent of coronary flow. Abstract Text:

R B Wambolt,M Grist,G P Bondy,M F Allard,

BACKGROUND: After ischemia, glycolysis and dysfunction are greater, while coupling of glucose oxidation to glycolysis is lower in hypertrophied hearts than in nonhypertrophied hearts. OBJECTIVE: To test the hypothesis that accelerated glycolysis, reduced coupling of glucose oxidation to glycolysis and increased postischemic dysfunction in hypertrophied hearts compared with nonhypertrophied hearts occur in the absence of differences in coronary flow. MATERIALS AND METHODS: Function, glycolysis and glucose oxidation were measured in isolated working control and hypertrophied rat hearts studied for 30 min before, and for 40 min after no flow global ischemia for 20 min under conditions in which coronary flow was comparable between the two groups. The hearts were perfused with 1.2 mmol/L palmitate, 5.5 mmol/L [5-3H/U-14C]-glucose, 0.5 mmol/L lactate, 100 mU/L insulin at a preload of 11.5 mmHg, and an afterload of 60 mmHg in control hearts or 80 mmHg in hypertrophied hearts. RESULTS: Despite comparable rates of coronary flow, functional recovery was lower in hypertrophied hearts than in control hearts. The rates of glycolysis were accelerated in hypertrophied hearts, while glucose oxidation did not significantly differ between the two groups. As a result, the coupling of glucose oxidation to glycolysis was lower in hypertrophied hearts than in control hearts. CONCLUSIONS: Increased postischemic dysfunction, accelerated glycolysis and reduced coupling of glucose oxidation to glycolysis in hypertrophied hearts compared with control hearts cannot be accounted for by differences in coronary flow. These data provide support for the concept that alterations in glucose metabolism contribute to the exaggerated postischemic dysfunction of hypertrophied hearts.

Accelerated glycolysis and greater postischemic dysfunction in hypertrophied rat hearts are independent of coronary flow. Publishing Authors By Initials

RB Wambolt,M Grist,GP Bondy,MF Allard,

For similar cardiovascular diseases: vascular diseases: reperfusion injury research abstracts see: cardiovascular diseases: vascular diseases: reperfusion injury research

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Accelerated glycolysis and greater postischemic dysfunction in hypertrophied rat hearts are independent of coronary flow. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Canadian journal of cardiology

VOLUME: 17

Page Numbers: 889-94

Journal Abbreviation:

ISSN: 1916-7075

DAY: 3

MONTH: Aug

YEAR: 2001

Accelerated glycolysis and greater postischemic dysfunction in hypertrophied rat hearts are independent of coronary flow. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8510280

Accelerated glycolysis and greater postischemic dysfunction in hypertrophied rat hearts are independent of coronary flow. Keywords Mesh Terms:

KEYWORDS: Reperfusion Injury

MESH TERMS: pathology

Chemical & Substance for Abstract: Accelerated glycolysis and greater postischemic dysfunction in hypertrophied rat hearts are independent of coronary flow. Information

Substance Name: Glucose

Registry Number: 50-99-7

Grant and Affiliation Information for Accelerated glycolysis and greater postischemic dysfunction in hypertrophied rat hearts are independent of coronary flow.

AFFILIATION: McDonald Research Laboratories/iCapture Center, Department of Pathology and Laboratory Medicine, University of British Columbia, St Paul's Hospital, 1081 Burrard Street, Vancouver, British Columbia V6Z 1Y6, Canada.

Country: Canada

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MEDLINETA: Can J Cardiol

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