Biological Impact of Transpulmonary Driving Pressure in Experimental Acute Respiratory Distress Syndrome

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52
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article
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2015
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LIPPINCOTT WILLIAMS & WILKINS
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SAMARY, Cynthia S.
SANTOS, Raquel S.
SANTOS, Cintia L.
FELIX, Nathane S.
BENTES, Maira
BARBOZA, Thiago
MORALES, Marcelo M.
GARCIA, Cristiane S. N. B.
SOUZA, Sergio A. L.
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ANESTHESIOLOGY, v.123, n.2, p.423-433, 2015
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Background: Ventilator-induced lung injury has been attributed to the interaction of several factors: tidal volume (V-T), positive end-expiratory pressure (PEEP), transpulmonary driving pressure (difference between transpulmonary pressure at end-inspiration and end-expiration, P,L), and respiratory system plateau pressure (Pplat,rs). Methods: Forty-eight Wistar rats received Escherichia coli lipopolysaccharide intratracheally. After 24h, animals were randomized into combinations of V-T and PEEP, yielding three different P,L levels: P,L-LOW (V-T = 6ml/kg, PEEP = 3cm H2O); P,L-MEAN (V-T = 13ml/kg, PEEP = 3cm H2O or V-T = 6ml/kg, PEEP = 9.5cm H2O); and P,L-HIGH (V-T = 22ml/kg, PEEP = 3cm H2O or V-T = 6ml/kg, PEEP = 11cm H2O). In other groups, at low V-T, PEEP was adjusted to obtain a Pplat,rs similar to that achieved with P,L-MEAN and P,L-HIGH at high V-T. Results: At P,L-LOW, expressions of interleukin (IL)-6, receptor for advanced glycation end products (RAGE), and amphiregulin were reduced, despite morphometric evidence of alveolar collapse. At P,L-HIGH (V-T = 6ml/kg and PEEP = 11cm H2O), lungs were fully open and IL-6 and RAGE were reduced compared with P,L-MEAN (27.412.9 vs. 41.6 +/- 14.1 and 0.6 +/- 0.2 vs. 1.4 +/- 0.3, respectively), despite increased hyperinflation and amphiregulin expression. At P,L-MEAN (V-T = 6ml/kg and PEEP = 9.5cm H2O), when PEEP was not high enough to keep lungs open, IL-6, RAGE, and amphiregulin expression increased compared with P,L-LOW (41.6 +/- 14.1 vs. 9.0 +/- 9.8, 1.4 +/- 0.3 vs. 0.6 +/- 0.2, and 6.7 +/- 0.8 vs. 2.2 +/- 1.0, respectively). At Pplat,rs similar to that achieved with P,L-MEAN and P,L-HIGH, higher V-T and lower PEEP reduced IL-6 and RAGE expression. Conclusion: In the acute respiratory distress syndrome model used in this experiment, two strategies minimized ventilator-induced lung injury: (1) low V-T and PEEP, yielding low P,L and Pplat,rs; and (2) low V-T associated with a PEEP level sufficient to keep the lungs open.
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  1. Moriondo A, 2012, RESP PHYSIOL NEUROBI, V181, P308, DOI 10.1016/j.resp.2012.03.013
  2. Uhlig S, 2004, AM J RESP CRIT CARE, V169, P314
  3. Servillo G, 1997, AM J RESP CRIT CARE, V155, P1629
  4. Laffey JG, 2004, INTENS CARE MED, V30, P347, DOI 10.1007/s00134-003-2051-1
  5. [Anonymous], 2000, NEW ENGL J MED, V342, P1301, DOI 10.1056/NEJM200005043421801
  6. Riva DR, 2008, CRIT CARE MED, V36, P1900, DOI 10.1097/CCM.0b013e3181760e5d
  7. Brower RG, 2004, NEW ENGL J MED, V351, P327
  8. Matute-Bello G, 2011, AM J RESP CELL MOL, V44, P725, DOI 10.1165/rcmb.2009-0210ST
  9. Ricard JD, 2001, AM J RESP CRIT CARE, V163, P1176
  10. BAYDUR A, 1982, AM REV RESPIR DIS, V126, P788
  11. Passaro CP, 2009, CRIT CARE MED, V37, P1011, DOI 10.1097/CCM.0b013e3181962d85
  12. Yamakawa N, 2011, AM J PHYSIOL-LUNG C, V300, pL516, DOI 10.1152/ajplung.00118.2010
  13. Borges JB, 2014, CRIT CARE MED, V42, pE279, DOI 10.1097/CCM.0000000000000161
  14. Monkman SL, 2004, CRIT CARE MED, V32, P2471, DOI 10.1097/01.CCM.0000147832.13213.1E
  15. Richard JCM, 2012, INTENS CARE MED, V38, P339, DOI 10.1007/s00134-012-2492-5
  16. Akamine R, 2007, J BIOCHEM BIOPH METH, V70, P481, DOI 10.1016/j.jbbm.2006.11.008
  17. MUSCEDERE JG, 1994, AM J RESP CRIT CARE, V149, P1327
  18. Protti A, 2013, CRIT CARE MED, V41, P1046, DOI 10.1097/CCM.0b013e31827417a6
  19. Wrigge H, 2004, ANESTH ANALG, V98, P775
  20. Chesnutt AN, 1997, AM J RESP CRIT CARE, V156, P840
  21. Farias LL, 2005, J APPL PHYSIOL, V98, P53, DOI 10.1152/japplphysiol.00118.2004
  22. Tsuchida S, 2006, AM J RESP CRIT CARE, V174, P279, DOI 10.1164/rccm.200506-1006OC
  23. Amato MBP, 1998, NEW ENGL J MED, V338, P347, DOI 10.1056/NEJM199802053380602
  24. Wakabayashi K, 2014, CRIT CARE MED, V42, pE49, DOI 10.1097/CCM.0b013e31829a822a
  25. Dreyfuss D, 1998, AM J RESP CRIT CARE, V157, P294
  26. Brochard L, 1998, AM J RESP CRIT CARE, V158, P1831
  27. Chiumello D, 1999, AM J RESP CRIT CARE, V160, P109
  28. RANIERI VM, 1991, AM REV RESPIR DIS, V144, P544
  29. Uhlig U, 2002, EUR RESPIR J, V20, P946, DOI 10.1183/09031936.02.01612001
  30. Spieth PM, 2011, BRIT J ANAESTH, V107, P388, DOI 10.1093/bja/aer144
  31. Briel M, 2010, JAMA-J AM MED ASSOC, V303, P865, DOI 10.1001/jama.2010.218
  32. Dolinay T, 2006, PHYSIOL GENOMICS, V26, P68, DOI 10.1152/physiolgenomics.00110.2005
  33. CRUZORIVE LM, 1990, AM J PHYSIOL, V258, pL148
  34. Dolinay T, 2008, PLOS ONE, V3, DOI 10.1371/journal.pone.0001601
  35. Chiumello D, 2013, CRIT CARE, V17, DOI 10.1186/cc13114
  36. Ko YA, 2013, RESP RES, V14, DOI 10.1186/1465-9921-14-69
  37. Reiss LK, 2011, PLOS ONE, V6, DOI 10.1371/journal.pone.0024527
  38. Santos CL, 2014, CRIT CARE, V18, DOI 10.1186/cc13920
  39. Silva PL, 2010, CRIT CARE, V14, DOI 10.1186/cc9063
  40. Thammanomai A, 2013, PLOS ONE, V8, DOI 10.1371/journal.pone.0053934