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(Circulation. 1999;99:1646-1649.)
© 1999 American Heart Association, Inc.

Correspondence

Limitations to the Assessment of Reperfusion Injury With Radiolabeled 2-Deoxyglucose

Torsten Doenst, MD

Department of Medicine Division of Cardiology, University of Texas–Houston Medical School, Houston, Tex

James E. Holden, PhD

Department of Medical Physics University of Wisconsin, Madison, Wis

Heinrich Taegtmeyer, MD, DPhil

Department of Medicine Division of Cardiology, University of Texas–Houston Medical School, Houston, Tex

	Introduction

 
To the Editor:

Matsumura et al¹ propose a new method to determine reperfusion injury in dog heart. The phosphorylation rate constant, k₃, for two 2-deoxyglucose moieties ([¹⁴C]2-DG and ¹⁸F-2-deoxy-2-fluro-D-glucose [FDG]) was compared with histological assessment of ischemic damage. The results suggest that a large portion of the infarcted myocardium loses viability during the first hours of reperfusion. If true, this would be the first demonstration of a bimodal time course of reperfusion injury in vivo.

Two factors may have affected the interpretation of the results. First, the assumption is made that the total ¹⁴C radioactivity in each sample is proportional to the phosphorylation rate. However, the contribution of unphosphorylated deoxyglucose, although declining, is never negligible, and in some circumstances, it can represent the majority of the tissue radioactivity. Correction for this is the main supposition of the deoxyglucose method.² Neglecting this correction is particularly problematic because the relationship between phosphorylated and unphosphorylated deoxyglucose concentrations is almost certain to be regionally variable.

Second, and more important, is the cancellation of the lumped constant (LC) from the calculations for the 2 tissue regions. We have shown that the LC is subject to considerable variability depending on the experimental conditions.³ It has been postulated that the LC is high when transport is rate limiting and low when phosphorylation is rate limiting.⁴ After 90 minutes of total ischemia, the available glucose in the ischemic area is likely to be very low. Any uptake of glucose at the onset of reperfusion is likely . . . [Full Text of this Article]

Richmond W. Jeremy, MBBS, PhD

Division of Cardiology Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Md, Department of Medicine, University of Sydney, Sydney, Australia

Kaname Matsumura, MD

Division of Nuclear Medicine Department of Radiology, Johns Hopkins Medical Institutions, Baltimore, Md, Department of Radiology, Mie University, Mie, Japan

Lewis C. Becker, MD

Division of Cardiology Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, Md

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