Inhaled Prostacyclin For The Treatment Of ARDS

  • Nicola Brienza
  • Marco V. Ranieri
Part of the NATO ASI Series book series (NSSA, volume 297)


Since 1967 the Acute Respiratory Distress Syndrome has represented a major cause of morbidity and mortality in the critical care setting. Many studies have been carried out over the past 30 years in the attempt to better define the pathophysiology of ARDS, but the overall result is that there is no single, clear-cut factor to which ARDS can be ascribed. At the present time, ARDS can be viewed as the pulmonary epiphenomenon of a systemic, multi-organ inflammatory response eliciting activation of a complex network of mediators. In the lung, such response causes non homogeneous permeability alterations and alveolar collapse with severe ventilationJperfusion mismatch. The mainstay of the inflammatory response is the pulmonary vascular endothelium activation and damage by lung injury mediators such as endotoxins, TNF-α, cytokines, arachidonic acid metabolites (1). The endothelial damage, with the loosening of the “tight junctions”, causes an increase of capillary leakage and a protein-enriched fluid engorgement of interstitial and alveolar spaces.


Nitric Oxide Pulmonary Hypertension Acute Respiratory Distress Syndrome Adult Respiratory Distress Syndrome Arachidonic Acid Metabolite 
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Copyright information

© Plenum Press, New York 1998

Authors and Affiliations

  • Nicola Brienza
    • 1
  • Marco V. Ranieri
    • 1
  1. 1.Istituto di Anestesiologia e RianimazioneUniversità di BariItaly

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