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  • Poster presentation
  • Open Access

Influence of the blood on the time course of pancreatitis-induced lung injury evaluated in isolated blood-perfused rat lungs

  • 1,
  • 1,
  • 1,
  • 1 and
  • 1
Critical Care200610 (Suppl 1) :P5

https://doi.org/10.1186/cc4352

  • Published:

Keywords

  • Pancreatitis
  • Lung Oedema
  • Endothelial Cell Injury
  • Taurocholic Acid
  • Homologous Blood

We evaluated the time course of pancreatitis-induced lung injury using an isolated blood-perfused rat lung preparation with lungs harvested 2, 6 or 18 hours after pancreatitis induced by injecting taurocholic acid into the pancreatic duct. This allowed us to separate and to determine the specific role of pancreatic blood vs normal blood on the expression of injury evidenced during isolated lung reperfusion. After 6 hours of pancreatitis (but not after 2 or 18 hours despite similar elevated serum amylase concentrations and persisting evidence of systemic inflammation) lung reperfusion with autologous blood or with homologous blood collected from normal rats revealed lung endothelial cell injury manifested by the formation of progressive lung oedema (~1 g/hour) accompanied by alterations in dynamic and static lung mechanics resulting in a final increased wet-to-dry lung weight ratio (7.5 ± 0.6; P < 0.01 vs control or time-matched sham-operated animals). In contrast, reperfusing normal lungs with pancreatic blood collected from rats 6 hours after taurocholate injection did not produce any alterations in lung weight and dynamic or static lung mechanics compared with normal control lungs. However, pancreatic blood collected 2 hours after taurocholate injection produced a moderate alteration in lung function but without significant increase in the wet-to-dry lung weight ratio (5.4 ± 0.5). Our results indicate that in this acute rat pancreatitis model lung injury occurred early, between 2 and 6 hours, and was completely reversible despite persistent elevated amylase concentration and systemic inflammation. Isolated lung reperfusion with normal homologous blood did not modify the expression of the pancreatic in-vivo-induced lung injury. Furthermore, pancreatic blood collected early (after 2 hours, but not after 6 hours) and used as perfusate for normal isolated lungs produced mild lung oedema and a moderate increase in dynamic lung compliance, suggesting that its potential toxic effects on the lungs were completely neutralized after 6 hours of pancreatitis.

Authors’ Affiliations

(1)
Centre Médical Universitaire, Genève, Switzerland

Copyright

© BioMed Central Ltd 2006

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