AJP - Heart and Circulatory Physiology, Vol 241, Issue 4 576-H582, Copyright © 1981 by American Physiological Society
Lack of a direct metabolic effect of fructose, 1,6-diphosphate in ischemic myocardium
L. J. Eddy, D. Chambers, S. Honig and J. M. Downey
Fructose 1,6-diphosphate (FdP) reportedly protects ischemic myocardium. To
determine whether this is a direct action on the heart, we used a canine
model in which two coronary arteries were perfused at identical but reduced
rates. Into one artery we infused FdP (total doses of 400 mg or 1.8 g)
while the other received 0.9% NaCl. After 1 h, biopsies were taken from a
normal region and the two ischemic regions and were analyzed for ATP,
phosphocreatine (PC), and lactate content. In the 0.9% NaCl-treated
ischemic tissue, ATP and PC fell to half the nonischemic levels. The
FdP-treated tissue exhibited high-energy phosphate levels similar to the
0.9% NaCl-treated tissue with no significant differences between the two
ischemic areas. Lactate levels in both ischemic areas were elevated
threefold above nonischemic levels. Contractility studies showed that
infusion of FdP directly into the coronary artery depressed contractility
in both nonischemic and ischemic conditions. Our data show that, if FdP
does have a protective action in ischemia, it is not through a direct
action on the heart.
