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Mechanical Ventilation Induces an Inflammatory Response in Preinjured Lungs in Late Phase of Sepsis.

Xuan W, Zhou Q, Yao S, Deng Q, Wang T, Wu Q - Oxid Med Cell Longev (2015)

Bottom Line: Interestingly, in the two groups where rats received low V T MV, we found that infiltration of inflammatory cells was only profound at day 4 after CLP.Marked elevation of protein leakage indicated a compromise in alveolar integrity in rats that received moderate V T MV at day 4 following CLP, correlating with architectural damage to the alveoli.Our study indicates that preinjured lungs are more sensitive to mechanical MV at later phases of sepsis, and this situation may be a result of differing immune status.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

ABSTRACT
Mechanical ventilation (MV) may amplify the lung-specific inflammatory response in preinjured lungs by elevating cytokine release and augmenting damage to the alveolar integrity. In this study, we test the hypothesis that MV exerts different negative impacts on inflammatory response at different time points of postlung injury. Basic lung injury was induced by cecal ligation and puncture (CLP) surgery in rats. Physiological indexes including blood gases were monitored during MV and samples were assessed following each experiment. Low V T (tidal volume) MV caused a slight increase in cytokine release and tissue damage at day 1 and day 4 after sepsis induced lung injury, while cytokine release from the lungs in the two moderately ventilated V T groups was amplified. Interestingly, in the two groups where rats received low V T MV, we found that infiltration of inflammatory cells was only profound at day 4 after CLP. Marked elevation of protein leakage indicated a compromise in alveolar integrity in rats that received moderate V T MV at day 4 following CLP, correlating with architectural damage to the alveoli. Our study indicates that preinjured lungs are more sensitive to mechanical MV at later phases of sepsis, and this situation may be a result of differing immune status.

No MeSH data available.


Related in: MedlinePlus

Total protein (a) and IL-6 (b) in BAL for each of the seven groups. ∗Without MV at the same day after CLP; #low VT MV at the same day after CLP. Data are presented as mean ± SD.
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fig5: Total protein (a) and IL-6 (b) in BAL for each of the seven groups. ∗Without MV at the same day after CLP; #low VT MV at the same day after CLP. Data are presented as mean ± SD.

Mentions: BALF total protein level was quantified to identify the status of capillary permeability and IL-6 was selected as a representative inflammatory cytokine. Studies have shown that moderate VT can augment rabbit lung cytokine release, such as TNF-α and IL-8, after the systemic of systemic LPS [18]. IL-6 is regarded as an active factor and an ongoing inflammatory marker of many lung diseases [19]. The synergistic role of IL-6 in pathologic mechanical stretch induced lung endothelial cell injury has also been demonstrated in vitro [20]. As shown in Figure 5, both total protein and IL-6 were significantly higher in group CLP4day + MMV when compared to groups CLP4day and CLP4day + LMV, which indicated that, on the fourth day after initiation of CLP, relatively higher volume of MV severely increases both lung capillary permeability and cytokine release. Furthermore, IL-6 was significantly higher in group CLP1day + MMV compared with groups CLP1day and CLP1day + LMV, while there were no statistically significant differences in total levels of protein observed between these groups (Figure 5). These results suggested that, at the early stage of sepsis (day one after CLP), when compared to low tidal volume, moderate tidal volume of MV changed inflammatory cytokine release but had no effect on lung capillary permeability.


Mechanical Ventilation Induces an Inflammatory Response in Preinjured Lungs in Late Phase of Sepsis.

Xuan W, Zhou Q, Yao S, Deng Q, Wang T, Wu Q - Oxid Med Cell Longev (2015)

Total protein (a) and IL-6 (b) in BAL for each of the seven groups. ∗Without MV at the same day after CLP; #low VT MV at the same day after CLP. Data are presented as mean ± SD.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4487711&req=5

fig5: Total protein (a) and IL-6 (b) in BAL for each of the seven groups. ∗Without MV at the same day after CLP; #low VT MV at the same day after CLP. Data are presented as mean ± SD.
Mentions: BALF total protein level was quantified to identify the status of capillary permeability and IL-6 was selected as a representative inflammatory cytokine. Studies have shown that moderate VT can augment rabbit lung cytokine release, such as TNF-α and IL-8, after the systemic of systemic LPS [18]. IL-6 is regarded as an active factor and an ongoing inflammatory marker of many lung diseases [19]. The synergistic role of IL-6 in pathologic mechanical stretch induced lung endothelial cell injury has also been demonstrated in vitro [20]. As shown in Figure 5, both total protein and IL-6 were significantly higher in group CLP4day + MMV when compared to groups CLP4day and CLP4day + LMV, which indicated that, on the fourth day after initiation of CLP, relatively higher volume of MV severely increases both lung capillary permeability and cytokine release. Furthermore, IL-6 was significantly higher in group CLP1day + MMV compared with groups CLP1day and CLP1day + LMV, while there were no statistically significant differences in total levels of protein observed between these groups (Figure 5). These results suggested that, at the early stage of sepsis (day one after CLP), when compared to low tidal volume, moderate tidal volume of MV changed inflammatory cytokine release but had no effect on lung capillary permeability.

Bottom Line: Interestingly, in the two groups where rats received low V T MV, we found that infiltration of inflammatory cells was only profound at day 4 after CLP.Marked elevation of protein leakage indicated a compromise in alveolar integrity in rats that received moderate V T MV at day 4 following CLP, correlating with architectural damage to the alveoli.Our study indicates that preinjured lungs are more sensitive to mechanical MV at later phases of sepsis, and this situation may be a result of differing immune status.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

ABSTRACT
Mechanical ventilation (MV) may amplify the lung-specific inflammatory response in preinjured lungs by elevating cytokine release and augmenting damage to the alveolar integrity. In this study, we test the hypothesis that MV exerts different negative impacts on inflammatory response at different time points of postlung injury. Basic lung injury was induced by cecal ligation and puncture (CLP) surgery in rats. Physiological indexes including blood gases were monitored during MV and samples were assessed following each experiment. Low V T (tidal volume) MV caused a slight increase in cytokine release and tissue damage at day 1 and day 4 after sepsis induced lung injury, while cytokine release from the lungs in the two moderately ventilated V T groups was amplified. Interestingly, in the two groups where rats received low V T MV, we found that infiltration of inflammatory cells was only profound at day 4 after CLP. Marked elevation of protein leakage indicated a compromise in alveolar integrity in rats that received moderate V T MV at day 4 following CLP, correlating with architectural damage to the alveoli. Our study indicates that preinjured lungs are more sensitive to mechanical MV at later phases of sepsis, and this situation may be a result of differing immune status.

No MeSH data available.


Related in: MedlinePlus