Display options
Cite
Henderson WR, Barnbrook J, Dominelli PB, et al. Administration of intrapulmonary sodium polyacrylate to induce lung injury for the development of a porcine model of early acute respiratory distress syndrome. Intensive Care Med Exp. 2014;2(1):5doi: 10.1186/2197-425X-2-5.
Henderson, W. R., Barnbrook, J., Dominelli, P. B., Griesdale, D. E., Arndt, T., Molgat-Seon, Y., Foster, G., Ackland, G. L., Xu, J., Ayas, N. T., & Sheel, A. W. (2014). Administration of intrapulmonary sodium polyacrylate to induce lung injury for the development of a porcine model of early acute respiratory distress syndrome. Intensive care medicine experimental, 2(1), 5. https://doi.org/10.1186/2197-425X-2-5
Henderson, William R, et al. "Administration of intrapulmonary sodium polyacrylate to induce lung injury for the development of a porcine model of early acute respiratory distress syndrome." Intensive care medicine experimental vol. 2,1 (2014): 5. doi: https://doi.org/10.1186/2197-425X-2-5
Henderson WR, Barnbrook J, Dominelli PB, Griesdale DE, Arndt T, Molgat-Seon Y, Foster G, Ackland GL, Xu J, Ayas NT, Sheel AW. Administration of intrapulmonary sodium polyacrylate to induce lung injury for the development of a porcine model of early acute respiratory distress syndrome. Intensive Care Med Exp. 2014 Dec;2(1):5. doi: 10.1186/2197-425X-2-5. Epub 2014 Feb 26. PMID: 26266906; PMCID: PMC4513039.
Copy Download .nbib Format: NLM
Share it on

Intensive Care Med Exp. 2014 Dec;2(1):5. doi: 10.1186/2197-425X-2-5. Epub 2014 Feb 26.

Administration of intrapulmonary sodium polyacrylate to induce lung injury for the development of a porcine model of early acute respiratory distress syndrome.

Intensive care medicine experimental

William R Henderson, Julian Barnbrook, Paolo B Dominelli, Donald Eg Griesdale, Tara Arndt, Yannick Molgat-Seon, Glen Foster, Gareth L Ackland, James Xu, Najib T Ayas, Andrew W Sheel

Affiliations

  1. Wolfson Institute for Biomedical Research, Department of Medicine, University College London, London, WC1E 6BT, UK, [email protected].

PMID: 26266906 PMCID: PMC4513039 DOI: 10.1186/2197-425X-2-5

Abstract

BACKGROUND: The loss of alveolar epithelial and endothelial integrity is a central component in acute respiratory distress syndrome (ARDS); however, experimental models investigating the mechanisms of epithelial injury are lacking. The purpose of the present study was to design and develop an experimental porcine model of ARDS by inducing lung injury with intrapulmonary administration of sodium polyacrylate (SPA).

METHODS: The present study was performed at the Centre for Comparative Medicine, University of British Columbia, Vancouver, British Columbia. Human alveolar epithelial cells were cultured with several different concentrations of SPA; a bioluminescence technique was used to assess cell death associated with each concentration. In the anesthetized pig model (female Yorkshire X pigs (n = 14)), lung injury was caused in 11 animals (SPA group) by injecting sequential aliquots (5 mL) of 1% SPA gel in aqueous solution into the distal airway via a rubber catheter through an endotracheal tube. The SPA was dispersed throughout the lungs by manual bag ventilation. Three control animals (CON group) underwent all experimental procedures and measurements with the exception of SPA administration.

RESULTS: The mean (± SD) ATP concentration after incubation of human alveolar epithelial cells with 0.1% SPA (0.92 ± 0.27 μM/well) was approximately 15% of the value found for the background control (6.30 ± 0.37 μM/well; p < 0.001). Elastance of the respiratory system (E RS) and the lung (E L) increased in SPA-treated animals after injury (p = 0.003 and p < 0.001, respectively). Chest wall elastance (E CW) did not change in SPA-treated animals. There were no differences in E RS, E L, or E CW in the CON group when pre- and post-injury values were compared. Analysis of bronchoalveolar lavage fluid showed a significant shift toward neutrophil predominance from before to after injury in SPA-treated animals (p < 0.001) but not in the CON group (p = 0.38). Necropsy revealed marked consolidation and congestion of the dorsal lung lobes in SPA-treated animals, with light-microscopy evidence of bronchiolar and alveolar spaces filled with neutrophilic infiltrate, proteinaceous debris, and fibrin deposition. These findings were absent in animals in the CON group. Electron microscopy of lung tissue from SPA-treated animals revealed injury to the alveolar epithelium and basement membranes, including intra-alveolar neutrophils and fibrin on the alveolar surface and intravascular fibrin (microthrombosis).

CONCLUSIONS: In this particular porcine model, the nonimmunogenic polymer SPA caused a rapid exudative lung injury. This model may be useful to study ARDS caused by epithelial injury and inflammation.

References

  1. Pathol Res Pract. 2002;198(5):355-61 - PubMed
  2. Crit Care Med. 1984 Dec;12(12):1044-8 - PubMed
  3. Am J Respir Crit Care Med. 1994 Jan;149(1):245-60 - PubMed
  4. Anesthesiology. 2001 May;94(5):862-9 - PubMed
  5. N Engl J Med. 2008 Feb 28;358(9):877-87 - PubMed
  6. Intensive Care Med. 2003 Nov;29(11):1943-9 - PubMed
  7. J Immunol Methods. 1993 Mar 15;160(1):81-8 - PubMed
  8. Respir Physiol Neurobiol. 2012 Mar 15;180(2-3):162-72 - PubMed
  9. JAMA. 2012 Jun 20;307(23):2526-33 - PubMed
  10. Chest. 2004 Aug;126(2):552-8 - PubMed
  11. Intensive Care Med. 2007 Dec;33(12):2109-15 - PubMed
  12. Crit Care Med. 2001 Nov;29(11):2176-84 - PubMed
  13. Intensive Care Med. 2001 Mar;27(3):477-85 - PubMed
  14. Vet Anaesth Analg. 2007 Sep;34(5):331-8 - PubMed
  15. Exp Lung Res. 2012 Jun;38(5):266-76 - PubMed
  16. Am J Respir Crit Care Med. 2011 May 15;183(10 ):1354-62 - PubMed
  17. Am J Respir Cell Mol Biol. 2011 May;44(5):725-38 - PubMed
  18. Intensive Care Med. 2001 Mar;27(3):457-60 - PubMed
  19. Crit Care Med. 2008 Jun;36(6):1900-8 - PubMed
  20. J Appl Physiol Respir Environ Exerc Physiol. 1984 Nov;57(5):1498-501 - PubMed
  21. Am J Physiol Lung Cell Mol Physiol. 2008 Sep;295(3):L379-99 - PubMed
  22. Crit Care. 2008;12(6):R145 - PubMed
  23. J Appl Toxicol. 1995 Jan-Feb;15(1):69-73 - PubMed
  24. Am J Respir Crit Care Med. 2001 May;163(6):1376-83 - PubMed
  25. J Appl Physiol (1985). 2005 May;98(5):1777-83 - PubMed
  26. Proc Am Thorac Soc. 2005;2(3):214-20 - PubMed
  27. J Exp Med. 2008 Dec 22;205(13):3065-77 - PubMed
  28. Am Rev Respir Dis. 1980 Jul;122(1):123-43 - PubMed
  29. Am J Respir Crit Care Med. 2001 Apr;163(5):1176-80 - PubMed
  30. Surgery. 1956 Oct;40(4):665-70 - PubMed
  31. Br J Anaesth. 2012 Oct;109(4):584-94 - PubMed
  32. Am J Respir Crit Care Med. 2008 Aug 15;178(4):346-55 - PubMed
  33. N Engl J Med. 1970 Dec 31;283(27):1478-84 - PubMed
  34. J Appl Physiol (1985). 2006 Jan;100(1):98-106 - PubMed
  35. Ann Intern Med. 2004 Sep 21;141(6):460-70 - PubMed
  36. J Appl Toxicol. 1989 Jun;9(3):191-8 - PubMed
  37. Lung. 1990;168(2):79-92 - PubMed
  38. J Clin Invest. 1995 Jul;96(1):107-16 - PubMed
  39. J Control Release. 2011 Nov 30;152 Suppl 1:e260-2 - PubMed
  40. Respir Res. 2001;2(6):353-64 - PubMed
  41. Crit Care Med. 2011 Apr;39(4):818-26 - PubMed
  42. Res Vet Sci. 1997 Nov-Dec;63(3):215-7 - PubMed
  43. Annu Rev Pathol. 2011;6:147-63 - PubMed
  44. Am J Respir Crit Care Med. 1998 Jul;158(1):3-11 - PubMed
  45. Radiology. 1999 Nov;213(2):545-52 - PubMed
  46. Anesthesiology. 1992 Oct;77(4):772-8 - PubMed
  47. Crit Care Med. 2006 May;34(5):1389-94 - PubMed
  48. Am Rev Respir Dis. 1990 Dec;142(6 Pt 1):1250-7 - PubMed

Publication Types