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Decrease in lung nitric oxide production after peritonitis in mice with sickle cell disease.

Pablo Bartolucci1, Minh-Triet Ngo, Yves Beuzard

  • 1Unité INSERM U492-Université Paris XII, Créteil, and Laboratoire de Thérapie Génique Hématopoïétique, Hôpital Saint Louis, Paris, France.

Critical Care Medicine
|December 15, 2006
PubMed
Summary

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In sickle cell disease (SCD) mice, acute peritonitis impairs nitric oxide (NO) production, shifting the enzymatic balance towards NO inhibition. This defect contributes to vaso-occlusive complications and mortality, which can be reversed by NO inhalation.

Area of Science:

  • Hematology
  • Pulmonology
  • Pathophysiology

Background:

  • Nitric oxide (NO) bioavailability is crucial for managing vaso-occlusive episodes in sickle cell disease (SCD).
  • Sepsis often triggers vaso-occlusive crisis and acute chest syndrome in SCD patients.
  • The enzymatic balance between nitric oxide synthases (NOS) and arginases regulates NO production.

Purpose of the Study:

  • To investigate the impact of acute infectious peritonitis on the NOS/arginase balance in the lungs of transgenic (SAD) sickle cell mice.
  • To determine if peritonitis alters lung nitric oxide production and bioavailability in SAD mice.

Main Methods:

  • Controlled animal study using transgenic SAD mice and wild-type littermates.
  • Cecal ligation and puncture-induced peritonitis model.

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  • Analysis of nitric oxide synthase (NOS) and arginase expression, lung nitric oxide levels, and exhaled nitric oxide.

    • Main Results:

    • Peritonitis increased NOS and exhaled NO in control mice, indicating a shift towards NO synthesis.
    • SAD mice exhibited decreased NOS proteins, lung NO, and exhaled NO post-peritonitis, with increased arginase I, indicating a shift towards NO inhibition.
    • Peritonitis led to higher mortality in SAD mice, which was abolished by nitric oxide inhalation.

    Conclusions:

    • Acute peritonitis in SAD mice is characterized by impaired lung nitric oxide production and bioavailability.
    • This NO deficiency may contribute to the systemic and lung vaso-occlusive complications observed in sickle cell disease.
    • Targeting NO pathways could be a therapeutic strategy for managing infectious complications in SCD.