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Articles in PresS, published online ahead of print August 9, 2002
J Appl Physiol, 10.1152/jap.00304.2002
Submitted on April 8, 2002
Accepted on August 6, 2002
1 Division of Physiology, Hadassah Schools of Dental Medicine and Medicine, The Hebrew University, Jerusalem, Israel
2 Department of Physical Chemistry, Tel Aviv University, Tel Aviv, Israel
3 Department of Cardiology, Johns Hopkins University, Baltimore, Maryland, USA
4 Department of Cardiology, Hadassah University Hospital, Jerusalem, Israel
* To whom correspondence should be addressed. E-mail: horowitz{at}cc.huji.ac.il.
Based on our observations of energy sparing in heat-acclimated rat hearts, we investigated whether changes in pre-ischemic glycogen level, glycolytic rate and plasma thyroxine level mediate cardioprotection induced in these hearts during ischemic/reperfusion insults. Control (24°C, C), heat-acclimated (34°C, 30days, AC), acclimated-euthyroid (34°C+3ng/ml L-thyroxine, AT), and control hypothyroid (24°C +0.02% 6-n-propyl-2-thiouracil, CP) groups were studied. Pre-ischemic glycogen was higher in AC than in C hearts (39.0°8.5 vs 19.2°4.2(SEM) mmol 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 (IC) was lengthened and the fraction of hearts experiencing IC was lowered. Pulse pressure recovery was improved in AC compared to C animals before, but not after absolute Na-iodoacetate-induced glycolysis inhibition. AT hearts exhibited decreased ischemic tolerance, while induced hypothyroidism in controls improved cardiotolerance. Thus, higher pre-ischemic glycogen and slowed glycolysis are associated with hypothyroidism, are likely important mediators of the improved ischemic tolerance exhibited by AC hearts.
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