Accession Number:

ADA315633

Title:

Intratracheal Aerosolization of Endotoxin (LPS) in the Rat: A Comprehensive Animal Model to Study Adult Respiratory Distress Syndrome (ARDS).

Descriptive Note:

Final rept.,

Corporate Author:

PRINS MAURITS LABORATORIUM TNO RIJSWIJK (NETHERLANDS)

Report Date:

1996-08-01

Pagination or Media Count:

34.0

Abstract:

The Adult Respiratory Distress Syndrome ARDS is characterized by high- permeability pulmonary oedema containing plasma-derived proteins, decreased lung volumes, decreased compliance, and arterial hypoxaemia. ARDS results from a number of different causes, of which Gram-negative sepsis and endotoxin lipopolysaccharide, LPS from bacteria and aspiration are thought to be major causes to the development of this life-threatening syndrome 1, 2. Although insight into the clinical course of ARDS patients is increasing, the sequence of pathophysiological events remains poorly understood 3, 4, 5. Currently, it is becoming widely accepted that an inflammatory reaction occurs in the lungs, in which numerous cellular and humoral mechanisms are involved, including macrophages, neutrophils, platelets, coagulation and fibrinolytic systems 6. Activated alveolar macrophages AM may contribute to this inflammatory reaction by the in vivo production of reactive oxygen intermediates ROl and chemotactic cytokines, of which TNFct seems to be the major one 7, 8, 9. Some of the damage done by ROl in vivo is assumed to be due to hydroxyl radicals OH 10, 11 that emerge from the conversion of O2 and H2O2. Not only in vivo experiments were in favour of a potential role for TNFct in pulmonary damage 12, but also in vitro experiments supported these findings 13, 14. In vitro TNFct was capable of priming PMNs for secondary stimuli 15, 16, 17. In addition to the central role of ROl and TNFct, there is clear support for the involvement of a multimediator network that leads to lung tissue injury 18. During the development of ARDS, the generation of various mediators contribute to the development of severe lung damage.

Subject Categories:

  • Anatomy and Physiology
  • Medicine and Medical Research

Distribution Statement:

APPROVED FOR PUBLIC RELEASE