24 research outputs found
Effects of sevoflurane postconditioning on cell death, inflammation and TLR expression in human endothelial cells exposed to LPS
Background: Sevoflurane is an anesthetic agent which also participates in protective mechanisms in sepsis, likely
due to anti-inflammatory properties. A key tissue in sepsis is the endothelium, which expresses TLR2 and TLR4
receptors, known regulators of inflammatory mechanisms and potential therapeutic targets for this pathology. In
this context, we explored the effect of sevoflurane postconditioning in an in vitro sepsis model.
Methods: Primary cultures of human umbilical vein endothelial cells were used for two different experiments. In
the first set, cultures were placed in an airtight incubation chamber and exposed to different concentrations of
sevoflurane (0,1,3 or 7% vol,) for 1 hour. In the second set, lipopolysaccharide from Escherichia coli 0111:B4 (1 μg/
mL) was added to culture medium for 3 hours and cells were subsequently exposed to sevoflurane (0,1,3 or 7%
vol,) for 1 hour as explained before. In both cases, cell viability was measured by MTT and Trypan blue assays, TLR2
and TLR4 expression were analyzed by flow cytometry, and TNFα and IL-6 levels were quantified in cell culture
media by an immunoassay immediately after exposure, at 6 and 24 hours.
Results: Exposure to 3% sevoflurane decreased TLR2 at 24 hours and TLR4 at 6 and 24 hours (both p<0.05),
whereas exposure to 7% decreased TLR4 expression at 6 hours (p<0.05). Both 3 and 7% sevoflurane decreased
TNF-α and IL-6 levels at 24 hours (both p<0.05). In LPS-stimulated cultures, exposure to 3% sevoflurane was
cytoprotective at 6 and 24 hours (p<0.05) compared with control, and decreased TLR2 and TLR4 expression at 24
hours (p<0.05); whereas 7% decreased TLR4 expression at 24 hours (p<0.05). Both 3% and 7% sevoflurane
decreased TNF-α and IL-6 levels at 24 hours (both p<0.05).
Conclusions: Postconditioning with the halogenated anesthetic agent sevoflurane after LPS stimulation shows a
cytoprotective effect in an in vitro model, decreasing cell death and reducing TLR2 and TLR4 expression as well as
levels of the inflammatory mediators TNF-α and IL-6 in human endothelial cellsS
Endotoxin-induced lung alveolar cell injury causes brain cell damage
Instituto de Salud Carlos III (ISCIII
Effects of sevoflurane postconditioning on cell death, inflammation and TLR expression in human endothelial cells exposed to LPS
Background: Sevoflurane is an anesthetic agent which also participates in protective mechanisms in sepsis, likely due to anti-inflammatory properties. A key tissue in sepsis is the endothelium, which expresses TLR2 and TLR4 receptors, known regulators of inflammatory mechanisms and potential therapeutic targets for this pathology. In this context, we explored the effect of sevoflurane postconditioning in an in vitro sepsis model.
Methods: Primary cultures of human umbilical vein endothelial cells were used for two different experiments. In the first set, cultures were placed in an airtight incubation chamber and exposed to different concentrations of sevoflurane (0,1,3 or 7% vol,) for 1 hour. In the second set, lipopolysaccharide from Escherichia coli 0111:B4 (1 μg/mL) was added to culture medium for 3 hours and cells were subsequently exposed to sevoflurane (0,1,3 or 7% vol,) for 1 hour as explained before. In both cases, cell viability was measured by MTT and Trypan blue assays, TLR2 and TLR4 expression were analyzed by flow cytometry, and TNFα and IL-6 levels were quantified in cell culture media by an immunoassay immediately after exposure, at 6 and 24 hours.
Results: Exposure to 3% sevoflurane decreased TLR2 at 24 hours and TLR4 at 6 and 24 hours (both p<0.05), whereas exposure to 7% decreased TLR4 expression at 6 hours (p<0.05). Both 3 and 7% sevoflurane decreased TNF-α and IL-6 levels at 24 hours (both p<0.05). In LPS-stimulated cultures, exposure to 3% sevoflurane was cytoprotective at 6 and 24 hours (p<0.05) compared with control, and decreased TLR2 and TLR4 expression at 24 hours (p<0.05); whereas 7% decreased TLR4 expression at 24 hours (p<0.05). Both 3% and 7% sevoflurane decreased TNF-α and IL-6 levels at 24 hours (both p<0.05).
Conclusions: Postconditioning with the halogenated anesthetic agent sevoflurane after LPS stimulation shows a cytoprotective effect in an in vitro model, decreasing cell death and reducing TLR2 and TLR4 expression as well as levels of the inflammatory mediators TNF-α and IL-6 in human endothelial cells
Common variants of NFE2L2 gene predisposes to acute respiratory distress syndrome in patients with severe sepsis
Postoperative hyperbilirubinemia and Gilbert's syndrome in patients undergoing cardiac surgery
We report a series of seven patients with Gilbert's syndrome undergoing cardiac surgery. Early and transient increase of total, direct, and indirect bilirubin without other complications was observed. Although this is a benign process, we believe that this disease should be routinely included in the differential diagnosis of postoperative jaundice after cardiopulmonary bypass
Multiple system organ response induced by hyperoxia in a clinically relevant animal model of sepsis
Postoperative hyperbilirubinemia and Gilbert's syndrome in patients undergoing cardiac surgery
We report a series of seven patients with Gilbert's syndrome undergoing cardiac surgery. Early and transient increase of total, direct, and indirect bilirubin without other complications was observed. Although this is a benign process, we believe that this disease should be routinely included in the differential diagnosis of postoperative jaundice after cardiopulmonary bypass