Myocardial regions perfused through a coronary stenosis may cease contracting, but remain viable. Clinical observations suggest that increased glucose utilization may be an adaptive mechanism in such "hibernating" regions. In this study, we used a combination of 13 C-NMR spectroscopy, GC-MS analysis, and tissue biochemical measurements to track glucose through intracellular metabolism in intact dogs infused with [1-13 C]glucose during a 3-4-h period of acute ischemic hibernation.During low-flow ischemia [3-13 C]alanine enrichment was higher, relative to plasma [1-13 C]glucose enrichment, in ischemic than in nonischemic regions of the heart, suggesting a greater contribution of exogenous glucose to glycolytic flux in the ischemic region ( ف 72 vs. ف 28%, P Ͻ 0.01). Both the fraction of glycogen synthase present in the physiologically active glucose-6-phosphate-independent form (46 Ϯ 10 vs. 9 Ϯ 6%, P Ͻ 0.01) and the rate of incorporation of circulating glucose into glycogen (94 Ϯ 25 vs. 20 Ϯ 15 nmol/ gram/min, P Ͻ 0.01) were also greater in ischemic regions.
Measurement of steady state [4-13 C]glutamate/[3-13 C]alanine enrichment ratios demonstrated that glucose-derived pyruvate supported 26-36% of total tricarboxylic acid cycle flux in all regions, however, indicating no preference for glucose over fat as an oxidative substrate in the ischemic myocardium. Thus during sustained regional low-flow ischemia in vivo, the ischemic myocardium increases its utilization of exogenous glucose as a substrate. Upregulation is restricted to cytosolic utilization pathways, however (glycolysis and glycogen synthesis), and fat continues to be the major source of mitochondrial oxidative substrate. ( J. Clin. Invest. 1996. 98:62-69.)
Relative SPECT count density with either maximal or mean count profiles correlated well with relative myocardial blood flow. Compared with maximal count profiles, quantification with mean count profiles improved estimation of relative flow.
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