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F-18-FDG Kinetics Parameters Depend on the Mechanism of Injury in Early Experimental Acute Respiratory Distress Syndrome
Journal article   Open access   Peer reviewed

F-18-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, …
The Journal of nuclear medicine (1978), Vol.55(11), pp.1871-1877
11/01/2014
DOI: 10.2967/jnumed.114.140962
PMCID: PMC4258066
PMID: 25286924
url
https://doi.org/10.2967/jnumed.114.140962View
Published (Version of record) Open Access

Abstract

PET with F-18-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 F-18-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 [LPS+] group; n = 6) or not (lipopolysaccharide-negative group; n = 6). F-18-FDG PET emission scans were then acquired. F-18-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 polymerase chain reaction. Results: F-18-FDG uptake increased in LPS+ (P = 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 F-18-FDG uptake in the LPS+ group was related both to increases in the F-18-FDG phosphorylation rate (P < 0.05) and to distribution volume (P < 0.01). F-18-FDG distribution volume increased with infiltrating neutrophils (P < 0.001) and phosphorylation rate with the regional expression of IL-1 beta (P = 0.026), IL-8 (P = 0.011), and IL-10 (P = 0.023). Conclusion: Noninvasive F-18-FDG PET-derived parameters represent histologic and gene expression markers of early lung injury. Pulmonary metabolism assessed with F-18-FDG PET depends on the mechanism of injury and appears to be additive for endotoxemia and surfactant depletion. F-18-FDG PET may be a valuable imaging biomarker of early lung injury.
Life Sciences & Biomedicine Radiology, Nuclear Medicine & Medical Imaging Science & Technology

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