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Inability of fructose 1,6-diphosphate to reduce myocardial infarct size.

Abstract
Fructose 1,6-diphosphate has been reported to reduce ischemic damage following coronary artery occlusion. To further evaluate fructose 1,6-diphosphate, we studied its effect on myocardial infarct size in open-chest, anesthetized dogs. Twenty min following left anterior descending coronary artery ligation, the animals received a constant infusion of either normal saline or fructose 1,6-diphosphate. Six hours following coronary artery ligation, the animals were killed and the hearts were sectioned from base to apex. Area at risk, infarct size, and infarct size expressed as a percentage of the area at risk were determined. Fructose 1,6-diphosphate had no effect on the amount of necrosis following coronary artery ligation. The area of necrosis expressed as a percentage of the left ventricle was similar in control (26 +/- 3%) and treated groups (24 +/- 4%). The area of necrosis expressed as a percentage of the area at risk was also similar in control and treated groups. Thus, in this model of myocardial ischemia, fructose 1,6-diphosphate does not reduce myocardial infarct size.
AuthorsE J Brown Jr, L Erburu, R A Kloner
JournalJournal of medicine (J Med) Vol. 18 Issue 1 Pg. 43-53 ( 1987) ISSN: 0025-7850 [Print] United States
PMID3474341 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Fructosediphosphates
  • Hexosediphosphates
  • fructose-1,6-diphosphate
Topics
  • Animals
  • Dogs
  • Fructosediphosphates (therapeutic use)
  • Hexosediphosphates (therapeutic use)
  • Myocardial Infarction (drug therapy)

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