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Circulation. 1998;97:1009-1016

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(Circulation. 1998;97:1009-1016.)
© 1998 American Heart Association, Inc.


Basic Science Reports

Positron Emission Tomography Analysis of [1-11C]Acetate Kinetics in Short-term Hibernating Myocardium

Rainer Schulz, MD; Christian Kappeler, PhD; Heinz Coenen, PhD; Andreas Bockisch, MD, PhD; ; Gerd Heusch, MD

From the Department of Pathophysiology, Center of Internal Medicine (R.S., G.H.) and the Department of Nuclear Medicine, Center of Radiology (C.K., H.C., A.B.), University Essen, School of Medicine, FRG.

Correspondence to Gerd Heusch, MD, FESC, FACC, Department of Pathophysiology, Center of Internal Medicine, University Essen, School of Medicine, Hufelandstraße 55, 45122 Essen, FRG.

Background—Modeling of the time-[1-11C]acetate activity curve assumes a constant concentration of labeled tricarboxylic acid cycle intermediates and associated metabolites, such as glutamate and aspartate, which may, however, decrease in short-term hibernating myocardium.

Methods and Results—In 12 anesthetized pigs, [1-11C]acetate was injected as a bolus into the cannulated left anterior descending coronary artery during normoperfusion, inotropic stimulation, and early (5 to 45 minutes) and prolonged ischemia (60 to 90 minutes). Regional myocardial oxygen consumption (MO2, microliters per minute per gram) was measured, and the absence of necrosis was verified by triphenyl tetrazolium chloride staining. Inotropic stimulation increased MO2 from 52.5±7.4 to 195.4±36.2 (mean±SD) and the rate constant (kmono, minutes-1) of [1-11C]acetate clearance from 0.094±0.018 to 0.322±0.076. During early ischemia, MO2 and kmono were decreased to 24.3±8.5 and 0.061±0.011, respectively. Kmono closely correlated to MO2 during normoperfusion, inotropic stimulation, and early ischemia. In short-term hibernating myocardium, however, at an unchanged MO2, kmono increased toward control values (0.080±0.014). Myocardial glutamate and aspartate concentrations (biopsies) decreased to 47±26% and 77±18%; the peak count rate decreased to 66±22% of its respective control value. After correction for the decreases in glutamate and aspartate or in peak count rate, kmono was again decreased (0.050±0.016 or 0.052±0.014, respectively), and a close relationship to MO2 was restored.

Conclusions—Kmono correlates to MO2 in short-term hibernating myocardium when the decreases in aspartate and glutamate or in peak count rate are considered.


Key Words: tomography • ischemia, myocardial • hibernation, myocardial • metabolism




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