Impact of pressure profile and duration of recruitment maneuvers on morphofunctional and biochemical variables in experimental lung injury.
OBJECTIVE
To investigate the effects of the rate of airway pressure increase and duration of recruitment maneuvers on lung function and activation of inflammation, fibrogenesis, and apoptosis in experimental acute lung injury.


METHODS
Prospective, randomized, controlled experimental study.


METHODS
University research laboratory.


METHODS
Thirty-five Wistar rats submitted to acute lung injury induced by cecal ligation and puncture.


METHODS
After 48 hrs, animals were randomly distributed into five groups (seven animals each): 1) nonrecruited (NR); 2) recruitment maneuvers (RMs) with continuous positive airway pressure (CPAP) for 15 secs (CPAP15); 3) RMs with CPAP for 30 secs (CPAP30); 4) RMs with stepwise increase in airway pressure (STEP) to targeted maximum within 15 secs (STEP15); and 5) RMs with STEP within 30 secs (STEP30). To perform STEP RMs, the ventilator was switched to a CPAP mode and positive end-expiratory pressure level was increased stepwise. At each step, airway pressure was held constant. RMs were targeted to 30 cm H2O. Animals were then ventilated for 1 hr with tidal volume of 6 mL/kg and positive end-expiratory pressure of 5 cm H2O.


RESULTS
Blood gases, lung mechanics, histology (light and electronic microscopy), interleukin-6, caspase 3, and type 3 procollagen mRNA expressions in lung tissue. All RMs improved oxygenation and lung static elastance and reduced alveolar collapse compared to NR. STEP30 resulted in optimal performance, with: 1) improved lung static elastance vs. NR, CPAP15, and STEP15; 2) reduced alveolar-capillary membrane detachment and type 2 epithelial and endothelial cell injury scores vs. CPAP15 (p < .05); and 3) reduced gene expression of interleukin-6, type 3 procollagen, and caspase 3 in lung tissue vs. other RMs.


CONCLUSIONS
Longer-duration RMs with slower airway pressure increase efficiently improved lung function, while minimizing the biological impact on lungs.
Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Pedro L
PL
Silva
Lillian
L
Moraes
Raquel S
RS
Santos
Cynthia
C
Samary
Debora S
DS
Ornellas
Tatiana
T
Maron-Gutierrez
Marcelo M
MM
Morales
Felipe
F
Saddy
Vera L
VL
Capelozzi
Paolo
P
Pelosi
John J
JJ
Marini
Marcelo
M
Gama de Abreu
Patricia R M
PR
Rocco
D055371:Acute Lung Injury / Q000150:complications / Q000401:mortality / Q000473:pathology* / Q000628:therapy*; D000818:Animals; D053148:Caspase 3 / Q000032:analysis / Q000378:metabolism; D045422:Continuous Positive Airway Pressure / Q000379:methods*; D004195:Disease Models, Animal; D015850:Interleukin-6 / Q000032:analysis / Q000378:metabolism; D008168:Lung / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D046529:Microscopy, Electron, Transmission; D011347:Procollagen; D011650:Pulmonary Alveoli / Q000378:metabolism / Q000473:pathology; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015656:Respiratory Mechanics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012680:Sensitivity and Specificity; D018805:Sepsis / Q000150:complications; D015996:Survival Rate; D013997:Time Factors
D015850:Interleukin-6; D011347:Procollagen; D053148:Caspase 3