The Journal of Thoracic and Cardiovascular Surgery
Volume 137, Issue 4 , Pages 824-828 , April 2009

Exogenous surfactant attenuation of ischemia–reperfusion injury in the lung through alteration of inflammatory and apoptotic factors

  • Bart P. van Putte, PhD, MD

      Affiliations

    • Department of Intensive Care Medicine, University Medical Center, Utrecht, The Netherlands
    • Department of Cardiothoracic Surgery, St Antonius Hospital, Nieuwegein, The Netherlands
    • Corresponding Author InformationAddress for reprints: Bart P. van Putte, PhD, MD, Department of Cardiothoracic Surgery, St. Antonius Hospital, Koekoekslaan 1, Nieuwegein, The Netherlands.
    • ,
  • Pieter M. Cobelens, PhD

      Affiliations

    • Department of Intensive Care Medicine, University Medical Center, Utrecht, The Netherlands
    • Laboratory for Psychoneuroimmunology, University Medical Center, Utrecht, The Netherlands
    • ,
  • Niels van der Kaaij, PhD

      Affiliations

    • Department of Anaesthesiology, Erasmus Medical Center, Rotterdam, The Netherlands
    • ,
  • Burkhard Lachmann, PhD, MD

      Affiliations

    • Department of Anaesthesiology, Erasmus Medical Center, Rotterdam, The Netherlands
    • ,
  • Annemieke Kavelaars, PhD

      Affiliations

    • Laboratory for Psychoneuroimmunology, University Medical Center, Utrecht, The Netherlands
    • ,
  • Cobi J. Heijnen, PhD

      Affiliations

    • Laboratory for Psychoneuroimmunology, University Medical Center, Utrecht, The Netherlands
    • ,
  • Jozef Kesecioglu, PhD, MD

      Affiliations

    • Department of Intensive Care Medicine, University Medical Center, Utrecht, The Netherlands

Received 18 February 2008 ,Revised 21 July 2008 ,Accepted 28 August 2008.

  • Image Result

    Representative paraffin sections of rat lung tissue stained with hematoxylin and eosin as function of time for sham-operated group (sham), control group (saline+I+R), and groups with surfactant admini

    Representative paraffin sections of rat lung tissue stained with hematoxylin and eosin as function of time for sham-operated group (sham), control group (saline+I+R), and groups with surfactant administered before (surfactant+I+R) and after (I+surfactant+R) ischemia. Original magnification ×200.

  • Image Result
    Inducible nitric oxide (iNOS) concentrations as function of time. Inducible nitric oxide expression levels were assessed in total cell ysates resolved by 10% sodium dodecyl sulfate polyacrylamide gel

    Inducible nitric oxide (iNOS) concentrations as function of time. Inducible nitric oxide expression levels were assessed in total cell ysates resolved by 10% sodium dodecyl sulfate polyacrylamide gel electrophoresis and analyzed by Western blot. Data (mean ± SEM) were normalized to β-actin expression and depicted as percentage of control values (black bars). Insets are representative Western blots depicting immunodetectable inducible nitric oxide. ∗∗P < .01; ∗∗∗P < .001; N = 7 per group. sham; saline + I + R; surfactant + I + R; I + surfactant + R.

  • Image Result
    Interleukin 6 (IL-6) concentrations as function of time. Interleukin 6 levels were determined by standard enzyme-linked immunosorbent assay. ∗P < .05; ∗∗P < .01; N = 7 per group. sham; saline + I +

    Interleukin 6 (IL-6) concentrations as function of time. Interleukin 6 levels were determined by standard enzyme-linked immunosorbent assay. ∗P < .05; ∗∗P < .01; N = 7 per group. sham; saline + I + R; surfactant + I + R; I + surfactant + R.

  • Image Result
    Interleukin 10 (IL-10) concentrations as function of time. Interleukin 10 levels were determined by standard enzyme-linked immunosorbent assay. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; N = 7 per group. sham

    Interleukin 10 (IL-10) concentrations as function of time. Interleukin 10 levels were determined by standard enzyme-linked immunosorbent assay. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; N = 7 per group. sham; saline + I + R; surfactant + I + R; I + surfactant + R.

  • Image Result
    Effect of lung ischemia–reperfusion injury on cleaved caspase-3 expression as function of time. Cleaved caspase-3 expression levels were assessed in total cell lysates resolved by 15% sodium dodecyl s

    Effect of lung ischemia–reperfusion injury on cleaved caspase-3 expression as function of time. Cleaved caspase-3 expression levels were assessed in total cell lysates resolved by 15% sodium dodecyl sulfate polyacrylamide gel electrophoresis and analyzed by Western blot. Data (mean ± SEM) were normalized to β-actin expression and depicted as percentage of values in sham-operated group. Insets are representative Western blots depicting immunodetectable cleaved caspase-3. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; N = 7 per group. sham; saline + I + R; surfactant + I + R; I + surfactant + R.

PII: S0022-5223(08)01466-9

doi: 10.1016/j.jtcvs.2008.08.046

The Journal of Thoracic and Cardiovascular Surgery
Volume 137, Issue 4 , Pages 824-828 , April 2009

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