Treatment with 24 h-delayed normo- and hyperbaric oxygenation in severe sepsis induced by cecal ligation and puncture in rats
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Treatment with 24 h-delayed normo- and hyperbaric oxygenation in severe sepsis induced by cecal ligation and puncture in rats. / Bærnthsen, Nina Falcon; Hansen, Marco Bo; Wahl, Anna Mygind; Simonsen, Ulf; Hyldegaard, Ole.
In: Journal of Inflammation, Vol. 14, 27, 2017.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Treatment with 24 h-delayed normo- and hyperbaric oxygenation in severe sepsis induced by cecal ligation and puncture in rats
AU - Bærnthsen, Nina Falcon
AU - Hansen, Marco Bo
AU - Wahl, Anna Mygind
AU - Simonsen, Ulf
AU - Hyldegaard, Ole
PY - 2017
Y1 - 2017
N2 - Background: Septic shock remains a leading cause of death worldwide. Hyperbaric oxygen treatment (HBO2) has been shown to alter the inflammatory response during sepsis and to reduce mortality. A therapeutic window of HBO2treatment has been demonstrated experimentally, but optimal timing remains uncertain. We investigated the effects of 24 h delayed normobaric oxygen (NBO2) and HBO2treatment on the endogenous production of the inflammatory markers interleukin (IL)-6, tumor necrosis factor (TNF)-α and IL-10, and on mortality in rats with cecal ligation and puncture (CLP) induced sepsis.Method: Fifty-five male Sprague-Dawley rats underwent CLP and were randomized to the following groups: 1) HBO22.5 bar absolute pressure (pabs); 2) NBO21.0 bar pabs; 3) Control (no-treatment), and they were individually monitored for 72 h with intermittent blood sampling.Results: IL-6, TNF-α, and IL-10 were increased 24 h after the procedure, and IL-6 was significantly higher in non-survivors than in survivors. The level of IL-10 was significantly higher at hour 48 in the HBO2group compared to control (p = 0.01), but this was not the case at other time points. No other significant differences in cytokine levels were found for any group comparisons. Delayed NBO2and HBO2treatment failed to change the mortality in the animals.Conclusion: High levels of IL-6 in non-surviving animals with sepsis suggest that IL-6 is a potential biomarker. We found a significantly higher concentration of IL-10 in the HBO2group at hour 48 vs. control animals. However, 24 h-delayed treatment with HBO2did not change the levels of pro-inflammatory cytokines and survival, suggesting that earlier intervention may be required to obtain an anti-inflammatory effect.
AB - Background: Septic shock remains a leading cause of death worldwide. Hyperbaric oxygen treatment (HBO2) has been shown to alter the inflammatory response during sepsis and to reduce mortality. A therapeutic window of HBO2treatment has been demonstrated experimentally, but optimal timing remains uncertain. We investigated the effects of 24 h delayed normobaric oxygen (NBO2) and HBO2treatment on the endogenous production of the inflammatory markers interleukin (IL)-6, tumor necrosis factor (TNF)-α and IL-10, and on mortality in rats with cecal ligation and puncture (CLP) induced sepsis.Method: Fifty-five male Sprague-Dawley rats underwent CLP and were randomized to the following groups: 1) HBO22.5 bar absolute pressure (pabs); 2) NBO21.0 bar pabs; 3) Control (no-treatment), and they were individually monitored for 72 h with intermittent blood sampling.Results: IL-6, TNF-α, and IL-10 were increased 24 h after the procedure, and IL-6 was significantly higher in non-survivors than in survivors. The level of IL-10 was significantly higher at hour 48 in the HBO2group compared to control (p = 0.01), but this was not the case at other time points. No other significant differences in cytokine levels were found for any group comparisons. Delayed NBO2and HBO2treatment failed to change the mortality in the animals.Conclusion: High levels of IL-6 in non-surviving animals with sepsis suggest that IL-6 is a potential biomarker. We found a significantly higher concentration of IL-10 in the HBO2group at hour 48 vs. control animals. However, 24 h-delayed treatment with HBO2did not change the levels of pro-inflammatory cytokines and survival, suggesting that earlier intervention may be required to obtain an anti-inflammatory effect.
U2 - 10.1186/s12950-017-0173-4
DO - 10.1186/s12950-017-0173-4
M3 - Journal article
C2 - 29204105
VL - 14
JO - Journal of inflammation
JF - Journal of inflammation
SN - 1078-7852
M1 - 27
ER -
ID: 194653403