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

doi:10.2967/jnumed.114.140962

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 journal › Article › peer-review

37 Scopus citations

Abstract

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 language	English (US)
Pages (from-to)	1871-1877
Number of pages	7
Journal	Journal of Nuclear Medicine
Volume	55
Issue number	11
DOIs	https://doi.org/10.2967/jnumed.114.140962
State	Published - Nov 1 2014
Externally published	Yes

Keywords

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

ASJC Scopus subject areas

Radiology Nuclear Medicine and imaging

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10.2967/jnumed.114.140962

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@article{98b29d9be2a74321824d9f2c32101399,

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

abstract = "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.",

keywords = "Adult, Endotoxemia, Fluorodeoxyglucose F18, Positron emission tomography, Pulmonary edema, Respiratory distress syndrome",

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

note = "Publisher Copyright: {\textcopyright} 2014 by the Society of Nuclear Medicine and Molecular Imaging, Inc.",

year = "2014",

month = nov,

day = "1",

doi = "10.2967/jnumed.114.140962",

language = "English (US)",

volume = "55",

pages = "1871--1877",

journal = "Journal of Nuclear Medicine",

issn = "0161-5505",

publisher = "Society of Nuclear Medicine Inc.",

number = "11",

}

TY - JOUR

T1 - 18F-FDG kinetics parameters depend on the mechanism of injury in early experimental acute respiratory distress syndrome

AU - De Prost, Nicolas

AU - Feng, Yan

AU - Wellman, Tyler

AU - Tucci, Mauro R.

AU - Costa, Eduardo L.

AU - Musch, Guido

AU - Winkler, Tilo

AU - Harris, R. Scott

AU - Venegas, Jose G.

AU - Chao, Wei

AU - Vidal Melo, Marcos F.

PY - 2014/11/1

Y1 - 2014/11/1

N2 - 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.

AB - 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.

KW - Adult

KW - Endotoxemia

KW - Fluorodeoxyglucose F18

KW - Positron emission tomography

KW - Pulmonary edema

KW - Respiratory distress syndrome

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SN - 0161-5505

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JO - Journal of Nuclear Medicine

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IS - 11

ER -

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

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