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Intensive Care Medicine

, Volume 38, Issue 2, pp 240–247 | Cite as

Lung strain and biological response in mechanically ventilated patients

  • Adrián González-López
  • Emilio García-Prieto
  • Estefanía Batalla-Solís
  • Laura Amado-Rodríguez
  • Noelia Avello
  • Lluís Blanch
  • Guillermo M. AlbaicetaEmail author
Original

Abstract

Purpose

Lung tissue may exhibit a biochemical response to excessive deformation. Since strain has been proposed as a marker of such deformation, we studied the relationships between strain and matrix remodeling and inflammation markers in mechanically ventilated patients with and without acute lung injury (ALI).

Methods

Twenty-two ventilated patients were studied (16 with ALI, 6 controls). Clinical data, gas exchange and respiratory mechanics were recorded, and end-expiratory lung volume (EELV) was measured by oxygen washin/washout. Extracellular matrix remodeling markers (procollagen, matrix metalloproteinases -2 and -9, TIMP-1) and inflammation markers (IL-6, IL-8, IL-10, IFNγ, IL-17A, and VEGF) were measured in bronchoalveolar lavage fluid (BALF). Strain was computed as the ratio between tidal volume and EELV. Patients with ALI were divided into two subgroups according to the median strain value (0.27).

Results

Patients in the ALI group exhibited higher airway pressures, lower EELV and higher strain than the control group. There were no significant differences in gas exchange, respiratory mechanics, or the matrix remodeling markers between ALI patients with normal and high strain. The subgroup of patients with high strain showed a fourfold increase of IL-6 and IL-8 concentrations in BALF, compared with patients with ALI and normal strain or patients without ALI. In the whole sample, IL-6 and IL-8 concentrations in BALF were correlated with strain (Spearman’s ρ = 0.67 and 0.77, respectively).

Conclusions

Increased strain is associated with a proinflammatory lung response in patients with ALI.

Keywords

Acute lung injury Mechanical ventilation Strain End-expiratory lung volume Inflammatory response 

Notes

Acknowledgments

Study supported by a Grant from General Electric Healthcare and by FICYT (COF-08-20 and COF-11-40). AGL is the recipient of a grant from Universidad de Oviedo (UNOV-09-BECDOC). IUOPA is supported by Obra Social Cajastur. CIBER-Enfermedades Respiratorias is supported by Instituto de Salud Carlos III. The authors would like to thank Ana Salas and Estela Rodríguez for their invaluable help with cytokine measurements, and Pablo Martinez Camblor for his help with the statistical analysis.

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Copyright information

© Copyright jointly held by Springer and ESICM 2011

Authors and Affiliations

  • Adrián González-López
    • 1
  • Emilio García-Prieto
    • 2
  • Estefanía Batalla-Solís
    • 1
  • Laura Amado-Rodríguez
    • 2
  • Noelia Avello
    • 3
  • Lluís Blanch
    • 4
    • 5
  • Guillermo M. Albaiceta
    • 1
    • 2
    • 5
    Email author
  1. 1.Departamento de Biología FuncionalInstituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de OviedoOviedoSpain
  2. 2.Servicio de Medicina IntensivaHospital Universitario Central de AsturiasOviedoSpain
  3. 3.Bioquímica ClínicaHospital Universitario Central de AsturiasOviedoSpain
  4. 4.Corporació Sanitaria Parc TaulíUniversitat Autónoma de BarcelonaSabadellSpain
  5. 5.CIBER Enfermedades RespiratoriasInstituto de Salud Carlos IIIMadridSpain

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