Introduction
Materials and methods
Experimental preparation
Mechanical ventilation
Positron emission tomography imaging protocol and processing
Modeling of 18F-fluorodeoxyglucose kinetics
Experimental protocol
Histological analysis
Statistical analysis
Results
Baseline physiological variables
Injurious ventilation (n= 6) | Protective ventilation (n= 6) | |||
---|---|---|---|---|
Parameter | Baseline | After MV + ETX | Baseline | After MV + ETX |
VT, ml/kg | 18.6 ± 3.9b | 14.3 ± 4.4c | 8.1 ± 0.2 | 8.0 ± 0.2 |
RR, breaths/min | 19 ± 2b | 21 ± 3c | 25 ± 2 | 26 ± 2 |
PEEP, cmH2O | 0b | 0
a
| 17 ± 3 | 17 ± 2 |
Mean airway pressure, cmH2O | 10 ± 2b | 10 ± 1b | 20 ± 3 | 21 ± 2 |
FiO2 | 0.30 (0.30 to 0.35) | 0.35 (0.30 to 0.62) | 0.30 (0.30 to 0.40) | 0.30 (0.30 to 0.42) |
PaO2/FiO2, torrg | 255 ± 74c | 162 ± 67d | 351 ± 117 | 261 ± 112 |
PaCO2, torr | 33 (30 to 40) | 43 (41 to 46) | 39 (36 to 42) | 39 (33 to 43) |
Qs/Qt | 0.24 (0.03 to 0.49) | 0.60 (0.37 to 0.75) | 0.15 (0.07 to 0.36) | 0.37 (0.21 to 0.48) |
Crs, ml/cmH2O | 15.4 ± 6.8 | 11.4 ± 3.5 | 12.8 ± 2.7 | 12.2 ± 1.8 |
Heart rate, bpm | 188 ± 30c | 150 ± 41f | 120 ± 26 | 137 ± 34 |
Cardiac output, L/min | 4.3 ± 1.1 | 4.4 ± 0.7d | 3.3 ± 0.7 | 3.1 ± 0.5 |
MAP, mmHg | 92 ± 12 | 78 ± 13 | 87 ± 13 | 81 ± 13 |
MPAP, mmHg | 16 ± 9 | 21 ± 5d | 22 ± 6 | 32 ± 6e |
PVR, dyn/s/cm5 | 228 ± 97 | 313 ± 109b | 372 ± 108 | 579 ± 118f |
Blood neutrophil count (103/μl)g | 3.09 (1.32 to 3.96) | 0.23 (0.14 to 0.25)e | 1.80 (1.05 to 3.90) | 0.20 (0.02 to 2.17) |
Oxygenation, regional aeration and perfusion before endotoxin administration
Oxygenation, regional aeration and perfusion after endotoxin administration
18F-fluorodeoxyglucose uptake magnitude and topographical distribution
Regional lung histology and 18F-fluorodeoxyglucose uptake values
Injurious ventilation (n= 6) | Protective ventilation (n= 6) |
P
| |||
---|---|---|---|---|---|
Lung region | Ventral | Dorsal | Ventral | Dorsal | |
Alveolar edema (n = 3) | 1 [0 to 1] | 1 [1 to 1] | 0 [0 to 0] | 0 [0 to 0] | 0.32 |
Septal edema (n = 3) | 0 [0 to 0] | 0 [0 to 0] | 1 [0 to 1] | 1 [0 to 2] | 0.16 |
Alveolar hemorrhage (n = 3) | 0 [0 to 1] | 1 [1 to 1] | 0 [0 to 0] | 0 [0 to 0] | 0.16 |
Septal congestion (n = 3) | 0 [0 to 0] | 0 [0 to 0] | 1 [0 to 1] | 1 [0 to 1] | 0.99 |
Total score (n = 12) | 1 [0 to 2] | 1 [1 to 2] | 1 [0 to 2] | 1 [0 to 3] | 0.16 |
Discussion
Animal model
Early changes in regional 18F-fluorodeoxyglucose uptake during acute lung injury
Cellular factors contributing to 18F-fluorodeoxyglucose uptake
Factors associated with modulation of lung inflammation by a protective ventilation strategy
Methodological considerations and limitations
Conclusion
Key messages
-
At early stages of endotoxemic ALI, mechanical ventilation strategy influences the intensity and distribution of neutrophil inflammation in the lungs.
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Protective ventilation improved gas exchange and reduced inflammatory cell activity in dependent lung regions.
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The main cause of reduced inflammatory cell activity was lowered neutrophilic metabolic activity.