18F-FDG kinetics parameters depend on the mechanism of injury in early experimental acute respiratory distress syndrome

Nicolas De Prost, Yan Feng, Tyler Wellman, Mauro R. Tucci, Eduardo L. Costa, Guido Musch, Tilo Winkler, R. Scott Harris, Jose G. Venegas, Wei Chao, Marcos F. Vidal Melo

Research output: Contribution to journalArticlepeer-review

30 Scopus citations


PET with 18F-FDG allows for noninvasive assessment of regional lung metabolism reflective of neutrophilic inflammation. This study aimed at determining during early acute lung injury whether local 18F-FDG phosphorylation rate and volume of distribution were sensitive to the initial regional inflammatory response and whether they depended on the mechanism of injury: endotoxemia and surfactant depletion. Methods: Twelve sheep underwent homogeneous unilateral surfactant depletion (alveolar lavage) and were mechanically ventilated for 4 h (positive end-expiratory pressure, 10 cm H2O; plateau pressure, 30 cm H2O) while receiving intravenous endotoxin (lipopolysaccharide-positive [LPS1] group; n 5 6) or not (lipopolysaccharide-negative group; n 5 6). 18F-FDG PET emission scans were then acquired. 18F-FDG phosphorylation rate and distribution volume were calculated with a 4-compartment model. Lung tissue expression of inflammatory cytokines was measured using real-time quantitative reverse transcription polymerse chain reaction. Results: 18F-FDG uptake increased in LPS1 (P 5 0.012) and in surfactant-depleted sheep (P , 0.001). These increases were topographically heterogeneous, predominantly in dependent lung regions, and without interaction between alveolar lavage and LPS. The increase of 18F-FDGuptake in the LPS1groupwas related both to increases in the 18F-FDG phosphorylation rate (P , 0.05) and to distribution volume (P , 0.01). 18F-FDG distribution volume increased with infiltrating neutrophils (P,0.001) and phosphorylation ratewith the regional expression of IL-1β (P 5 0.026), IL-8 (P 5 0.011), and IL-10 (P 5 0.023). Conclusion: Noninvasive 18F-FDG PET-derived parameters represent histologic and gene expression markers of early lung injury. Pulmonary metabolism assessed with 18F-FDG PET depends on the mechanism of injury and appears to be additive for endotoxemia and surfactant depletion. 18F-FDG PET may be a valuable imaging biomarker of early lung injury.

Original languageEnglish
Pages (from-to)1871-1877
Number of pages7
JournalJournal of Nuclear Medicine
Issue number11
StatePublished - Nov 1 2014
Externally publishedYes


  • Adult
  • Endotoxemia
  • Fluorodeoxyglucose F18
  • Positron emission tomography
  • Pulmonary edema
  • Respiratory distress syndrome


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