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1 Division of Physiology, Hadassah Schools of Dental Medicine and Medicine, The Hebrew University, and 4 Department of Cardiology, Hadassah University Hospital, Jerusalem 91120; and 2 Department of Physical Chemistry, Tel Aviv University, Tel Aviv 69978, Israel; and 3 Division of Cardiology, Johns Hopkins Hospital, Baltimore, Maryland 21218
Based on our observations of
energy sparing in heat-acclimated (AC) rat hearts, we investigated
whether changes in preischemic glycogen level, glycolytic rate,
and plasma thyroxine level mediate cardioprotection induced in these
hearts during ischemia-reperfusion insults. Control (C)
(24°C), AC (34°C, 30 days), acclimated-euthyroid (34°C + 3 ng/ml L-thyroxine), and control hypothyroid (24°C + 0.02% 6-n-propyl-2-thiouracil) groups were studied.
Preischemic glycogen was higher in AC than in C hearts
[39.0 ± 8.5 vs. 19.2 ± 4.2 (SE) µmol glucose/g wet wt;
P < 0.0006], and the lactate produced vs. glycogen
level during total ischemia (13C-NMR spectroscopy)
was markedly slower (AC: 
0.82x, r = 0.98 vs. C: 4.7x, r = 0.9). Time to onset of
ischemic contracture was lengthened, and the fraction of
hearts experiencing ischemic contracture was lowered. Pulse
pressure recovery was improved in AC compared with C animals
before, but not after, absolute sodium iodoacetate-induced glycolysis
inhibition. Acclimated-euthyroid hearts exhibited decreased
ischemic tolerance, whereas induced hypothyroidism in C
improved cardiotolerance. Thus higher preischemic glycogen and
slowed glycolysis are associated with hypothyroidism and are likely
important mediators of the improved ischemic tolerance exhibited by AC hearts.
ischemia; hypothyroidism; [13C]glucose nuclear magnetic resonance spectroscopy; glycolytic flux; rat
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