Lung inflammation persists after 27 hours of protective Acute Respiratory Distress Syndrome Network Strategy and is concentrated in the nondependent lung.
OBJECTIVE
PET with [18F]fluoro-2-deoxy-D-glucose can be used to image cellular metabolism, which during lung inflammation mainly reflects neutrophil activity, allowing the study of regional lung inflammation in vivo. We aimed at studying the location and evolution of inflammation by PET imaging, relating it to morphology (CT), during the first 27 hours of application of protective-ventilation strategy as suggested by the Acute Respiratory Distress Syndrome Network, in a porcine experimental model of acute respiratory distress syndrome.


METHODS
Prospective laboratory investigation.


METHODS
University animal research laboratory.


METHODS
Ten piglets submitted to an experimental model of acute respiratory distress syndrome.


METHODS
Lung injury was induced by lung lavages and 210 minutes of injurious mechanical ventilation using low positive end-expiratory pressure and high inspiratory pressures. During 27 hours of controlled mechanical ventilation according to Acute Respiratory Distress Syndrome Network strategy, the animals were studied with dynamic PET imaging of [18F]fluoro-2-deoxy-D-glucose at two occasions with 24-hour interval between them.


RESULTS
[18F]fluoro-2-deoxy-D-glucose uptake rate was computed for the total lung, four horizontal regions from top to bottom (nondependent to dependent regions) and for voxels grouped by similar density using standard Hounsfield units classification. The global lung uptake was elevated at 3 and 27 hours, suggesting persisting inflammation. In both PET acquisitions, nondependent regions presented the highest uptake (p = 0.002 and p = 0.006). Furthermore, from 3 to 27 hours, there was a change in the distribution of regional uptake (p = 0.003), with more pronounced concentration of inflammation in nondependent regions. Additionally, the poorly aerated tissue presented the largest uptake concentration after 27 hours.


CONCLUSIONS
Protective Acute Respiratory Distress Syndrome Network strategy did not attenuate global pulmonary inflammation during the first 27 hours after severe lung insult. The strategy led to a concentration of inflammatory activity in the upper lung regions and in the poorly aerated lung regions. The present findings suggest that the poorly aerated lung tissue is an important target of the perpetuation of the inflammatory process occurring during ventilation according to the Acute Respiratory Distress Syndrome Network strategy.
1Hedenstierna Laboratory, Department of Surgical Sciences, Section of Anaesthesiology & Critical Care, Uppsala University, Uppsala, Sweden. 2Pulmonary Division, Cardio-Pulmonary Department, Heart Institute (Incor), University of São Paulo, São Paulo, Brazil. 3Research and Education Institute, Hospital Sirio-Libanês, São Paulo, Brazil. 4Hedenstierna Laboratory, Department of Medical Sciences, Clinical Physiology, Uppsala University, Uppsala, Sweden. 5Intensive Care Department, Hospital San Matteo, Pavia, Italy. 6Department of Medical Physics, University Hospital, Uppsala, Sweden. 7Centros de Investigación Biomédica en Red de Enfermedades Respiratorias, Instituto de Salud Carlos III, Madrid, Spain.
João Batista
JB
Borges
Eduardo L V
EL
Costa
Maria
M
Bergquist
Luca
L
Lucchetta
Charles
C
Widström
Enn
E
Maripuu
Fernando
F
Suarez-Sipmann
Anders
A
Larsson
Marcelo B P
MB
Amato
Göran
G
Hedenstierna
D000818:Animals; D004195:Disease Models, Animal; D019788:Fluorodeoxyglucose F18; D008297:Male; D011014:Pneumonia / Q000000981:diagnostic imaging / Q000503:physiopathology*; D049268:Positron-Emission Tomography; D012121:Respiration, Artificial / Q000379:methods*; D013552:Swine; D055397:Ventilator-Induced Lung Injury / Q000000981:diagnostic imaging / Q000503:physiopathology*
D019788:Fluorodeoxyglucose F18