Effects of short-term propofol and dexmedetomidine on pulmonary morphofunction and biological markers in experimental mild acute lung injury

- Short-term intravenous administration of dexmedetomidine and propofol led to different functional effects and activation of biological markers in endotoxin-induced mild acute lung injury.
- Propofol reduced static lung elastance, resistive pressure, alveolar collapse and lower IL (interleukin)-6 and IL-1β expression compared to dexmedetomidine.
- Dexmedetomidine did not modify lung mechanics and histology, but improved oxygenation and decreased inducible nitric oxide and increased nuclear factor erythroid 2-related factor 2 expression in lung tissue.

We evaluated whether the short-term use of dexmedetomidine and propofol may attenuate inflammatory response and improve lung morphofunction in experimental acute lung injury (ALI). Thirty-six Wistar rats were randomly divided into five groups. Control (C) and ALI animals received sterile saline solution and Escherichia coli lipopolysaccharide by intraperitoneal injection respectively. After 24 h, ALI animals were randomly treated with dexmedetomidine, propofol, or thiopental sodium for 1 h. Propofol reduced static lung elastance and resistive pressure and was associated with less alveolar collapse compared to thiopental sodium and dexmedetomidine. Dexmedetomidine improved oxygenation, but did not modify lung mechanics or histology. Propofol was associated with lower IL (interleukin)-6 and IL-1β expression, whereas dexmedetomidine led to reduced inducible nitric oxide (iNOS) and increased nuclear factor erythroid 2-related factor 2 (Nrf2) expression in lung tissue compared to thiopental sodium. In conclusion, in this model of mild ALI, short-term use of dexmedetomidine and propofol led to different functional effects and activation of biological markers associated with pulmonary inflammation.