RATIONALE AND OBJECTIVES: Dynamic positron emission tomographic imaging of the radiotracer 2-deoxy-2-[(18)F]fluoro-D-glucose ((18)F-FDG) is increasingly used to assess metabolic activity of lung inflammatory cells. To analyze the kinetics of (18)F-FDG in brain and tumor tissues, the Sokoloff model has been typically used. In the lungs, however, a high blood-to-parenchymal volume ratio and (18)F-FDG distribution in edematous injured tissue could require a modified model to properly describe (18)F-FDG kinetics. MATERIALS AND METHODS: We developed and validated a new model of lung (18)F-FDG kinetics that includes an extravascular/noncellular compartment in addition to blood and (18)F-FDG precursor pools for phosphorylation. Parameters obtained from this model were compared with those obtained using the Sokoloff model. We analyzed dynamic PET data from 15 sheep with smoke or ventilator-induced lung injury. RESULTS: In the majority of injured lungs, the new model provided better fit to the data than the Sokoloff model. Rate of pulmonary (18)F-FDG net uptake and distribution volume in the precursor pool for phosphorylation correlated between the two models (R(2)=0.98, 0.78), but were overestimated with the Sokoloff model by 17% (P< .05) and 16% (P< .0005) compared to the new one. The range of the extravascular/noncellular (18)F-FDG distribution volumes was up to 13% and 49% of lung tissue volume in smoke- and ventilator-induced lung injury, respectively. CONCLUSION: The lung-specific model predicted (18)F-FDG kinetics during acute lung injury more accurately than the Sokoloff model and may provide new insights in the pathophysiology of lung injury.
RATIONALE AND OBJECTIVES: Dynamic positron emission tomographic imaging of the radiotracer 2-deoxy-2-[(18)F]fluoro-D-glucose ((18)F-FDG) is increasingly used to assess metabolic activity of lung inflammatory cells. To analyze the kinetics of (18)F-FDG in brain and tumor tissues, the Sokoloff model has been typically used. In the lungs, however, a high blood-to-parenchymal volume ratio and (18)F-FDG distribution in edematous injured tissue could require a modified model to properly describe (18)F-FDG kinetics. MATERIALS AND METHODS: We developed and validated a new model of lung (18)F-FDG kinetics that includes an extravascular/noncellular compartment in addition to blood and (18)F-FDG precursor pools for phosphorylation. Parameters obtained from this model were compared with those obtained using the Sokoloff model. We analyzed dynamic PET data from 15 sheep with smoke or ventilator-induced lung injury. RESULTS: In the majority of injured lungs, the new model provided better fit to the data than the Sokoloff model. Rate of pulmonary (18)F-FDG net uptake and distribution volume in the precursor pool for phosphorylation correlated between the two models (R(2)=0.98, 0.78), but were overestimated with the Sokoloff model by 17% (P< .05) and 16% (P< .0005) compared to the new one. The range of the extravascular/noncellular (18)F-FDG distribution volumes was up to 13% and 49% of lung tissue volume in smoke- and ventilator-induced lung injury, respectively. CONCLUSION: The lung-specific model predicted (18)F-FDG kinetics during acute lung injury more accurately than the Sokoloff model and may provide new insights in the pathophysiology of lung injury.
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