• Peter M Spieth, Pedro L Silva, Cristiane S N B Garcia, Debora S Ornellas, Cynthia S Samary, Lillian Moraes, Maira Bentes, Marcelo M Morales, Michael Kasper, Andreas Güldner, Robert Huhle, Thea Koch, Paolo Pelosi, Marcelo Gama de Abreu, and Patricia R M Rocco.
• From the Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Therapy, University Hospital Carl Gustav Carus, Dresden, Technische Universität Dresden, Dresden, Germany (P.M.S., A.G., R.H., T.K., M.G.d.A.); Laboratory of Pulmonary Investigation (P.L.S., C.S.N.B.G., D.S.O., C.S.S., L.M., M.B., P.R.M.R.), and Laboratory of Cellular and Molecular Biology (M.M.M.), Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil; Rio de Janeiro Federal Institute of Education, Science and Technology, Rio de Janeiro, Brazil (C.S.N.B.G.); Institute of Anatomy, Technical University Dresden, Dresden, Germany (M.K.); and IRCCS AOU San Martino-IST, Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, Genoa, Italy (P.P.).
• Anesthesiology. 2015 Jan 1;122(1):106-16.

BackgroundMechanical ventilation can lead to lung biotrauma when mechanical stress exceeds safety thresholds. The authors investigated whether the duration of mechanical stress, that is, the impact of a stress versus time product (STP), influences biotrauma. The authors hypothesized that higher STP levels are associated with increased inflammation and with alveolar epithelial and endothelial cell injury.MethodsIn 46 rats, Escherichia coli lipopolysaccharide (acute lung inflammation) or saline (control) was administered intratracheally. Both groups were protectively ventilated with inspiratory-to-expiratory ratios 1:2, 1:1, or 2:1 (n = 12 each), corresponding to low, middle, and high STP levels (STPlow, STPmid, and STPhigh, respectively). The remaining 10 animals were not mechanically ventilated.ResultsIn animals with mild acute lung inflammation, but not in controls: (1) messenger RNA expression of interleukin-6 was higher in STPhigh (28.1 ± 13.6; mean ± SD) and STPlow (28.9 ± 16.0) versus STPmid (7.4 ± 7.5) (P < 0.05); (2) expression of the receptor for advanced glycation end-products was increased in STPhigh (3.6 ± 1.6) versus STPlow (2.3 ± 1.1) (P < 0.05); (3) alveolar edema was decreased in STPmid (0 [0 to 0]; median, Q1 to Q3) compared with STPhigh (0.8 [0.6 to 1]) (P < 0.05); and (4) expressions of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 were higher in STPlow (3.0 ± 1.8) versus STPhigh (1.2 ± 0.5) and STPmid (1.4 ± 0.7) (P < 0.05), respectively.ConclusionsIn the mild acute lung inflammation model used herein, mechanical ventilation with inspiratory-to-expiratory of 1:1 (STPmid) minimized lung damage, whereas STPhigh increased the gene expression of biological markers associated with inflammation and alveolar epithelial cell injury and STPlow increased markers of endothelial cell damage.

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