Inability of fructose 1,6-diphosphate to reduce myocardial infarct size.
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.
D000818:Animals; D004285:Dogs; D005635:Fructosediphosphates / Q000627:therapeutic use*; D006598:Hexosediphosphates / Q000627:therapeutic use*; D009203:Myocardial Infarction / Q000188:drug therapy*
D005635:Fructosediphosphates; D006598:Hexosediphosphates; C029063:fructose-1,6-diphosphate