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Short-term hyperoxia does not exert immunologic effects during experimental murine and human endotoxemia.

Kiers D, Gerretsen J, Janssen E, John A, Groeneveld R, van der Hoeven JG, Scheffer GJ, Pickkers P, Kox M - Sci Rep (2015)

Bottom Line: Here, we demonstrate that, in the absence of systemic inflammation, short-term hyperoxia (100% O2 for 2.5 hours in mice and 3.5 hours in humans) does not result in increased levels of inflammatory cytokines in both mice and healthy volunteers.Furthermore, we show that, compared with room air, hyperoxia does not affect the systemic inflammatory response elicited by administration of bacterial endotoxin in mice and man.Our results indicate that hyperoxia does not exert direct anti-inflammatory effects and temper expectations of using it as an immunomodulatory treatment strategy.

View Article: PubMed Central - PubMed

Affiliation: Department of Intensive Care Medicine, Radboud university medical center, Geert Grooteplein Zuid 10, Nijmegen, 6500 HB, Netherlands.

ABSTRACT
Oxygen therapy to maintain tissue oxygenation is one of the cornerstones of critical care. Therefore, hyperoxia is often encountered in critically ill patients. Epidemiologic studies have demonstrated that hyperoxia may affect outcome, although mechanisms are unclear. Immunologic effects might be involved, as hyperoxia was shown to attenuate inflammation and organ damage in preclinical models. However, it remains unclear whether these observations can be ascribed to direct immunosuppressive effects of hyperoxia or to preserved tissue oxygenation. In contrast to these putative anti-inflammatory effects, hyperoxia may elicit an inflammatory response and organ damage in itself, known as oxygen toxicity. Here, we demonstrate that, in the absence of systemic inflammation, short-term hyperoxia (100% O2 for 2.5 hours in mice and 3.5 hours in humans) does not result in increased levels of inflammatory cytokines in both mice and healthy volunteers. Furthermore, we show that, compared with room air, hyperoxia does not affect the systemic inflammatory response elicited by administration of bacterial endotoxin in mice and man. Finally, neutrophil phagocytosis and ROS generation are unaffected by short-term hyperoxia. Our results indicate that hyperoxia does not exert direct anti-inflammatory effects and temper expectations of using it as an immunomodulatory treatment strategy.

No MeSH data available.


Related in: MedlinePlus

Blood gas parameters, hemodynamics, and temperature in healthyvolunteers.(a) arterial oxygen pressure (PaO2), (b) arterialcarbon dioxide pressure (PaCO2), (c) mean arterialpressure (MAP), (d) heart rate, and (e) tympanic temperature.The period of hyperoxia or normoxia is indicated with a grey box. In theendotoxemia groups, LPS was administered atT = 0 hours. Data are expressed asmean ± SEM. NORM-E: normoxicendotoxemia, HYPER-E: hyperoxic endotoxemia, HYPER: hyperoxia.
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f2: Blood gas parameters, hemodynamics, and temperature in healthyvolunteers.(a) arterial oxygen pressure (PaO2), (b) arterialcarbon dioxide pressure (PaCO2), (c) mean arterialpressure (MAP), (d) heart rate, and (e) tympanic temperature.The period of hyperoxia or normoxia is indicated with a grey box. In theendotoxemia groups, LPS was administered atT = 0 hours. Data are expressed asmean ± SEM. NORM-E: normoxicendotoxemia, HYPER-E: hyperoxic endotoxemia, HYPER: hyperoxia.

Mentions: During the hyperoxic/normoxic period, mean PaO2 was similar in thehyperoxia group and hyperoxic endotoxemia group(54.8 ± 3.0(411.7 ± 22.8) and54.1 ± 4.1(405.9 ± 31.1) kPa (mmHg),p = 0.89), whereas PaO2 in the hyperoxicendotoxemia group was higher than in the normoxic endotoxemia group(15.2 ± 0.7(114.3 ± 5.5) kPa,p < 0.0001, Fig. 2a).PaCO2 was 5.0 ± 0.3(37.8 ± 1.9) kPa in the hyperoxia group,5.5 ± 0.2(40.9 ± 1.2) kPa in the hyperoxicendotoxemia group, and 5.3 ± 0.2(39.5 ± 1.7) kPa in the normoxicendotoxemia group (Fig. 2b). After an initialincrease, PaCO2 decreased over time in the hyperoxia group. Asimilar pattern was observed in the normoxic endotoxemia and hyperoxicendotoxemia groups, with no differences between these groups (Fig. 2b). Lactate levels were in the normal range(<2 mmol/L) throughout the experiment in all subjects. Inall groups, mean arterial pressure (MAP) decreased over time, with nodifference between the normoxic and hyperoxic endotoxemia groups (Fig. 2c).


Short-term hyperoxia does not exert immunologic effects during experimental murine and human endotoxemia.

Kiers D, Gerretsen J, Janssen E, John A, Groeneveld R, van der Hoeven JG, Scheffer GJ, Pickkers P, Kox M - Sci Rep (2015)

Blood gas parameters, hemodynamics, and temperature in healthyvolunteers.(a) arterial oxygen pressure (PaO2), (b) arterialcarbon dioxide pressure (PaCO2), (c) mean arterialpressure (MAP), (d) heart rate, and (e) tympanic temperature.The period of hyperoxia or normoxia is indicated with a grey box. In theendotoxemia groups, LPS was administered atT = 0 hours. Data are expressed asmean ± SEM. NORM-E: normoxicendotoxemia, HYPER-E: hyperoxic endotoxemia, HYPER: hyperoxia.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4663498&req=5

f2: Blood gas parameters, hemodynamics, and temperature in healthyvolunteers.(a) arterial oxygen pressure (PaO2), (b) arterialcarbon dioxide pressure (PaCO2), (c) mean arterialpressure (MAP), (d) heart rate, and (e) tympanic temperature.The period of hyperoxia or normoxia is indicated with a grey box. In theendotoxemia groups, LPS was administered atT = 0 hours. Data are expressed asmean ± SEM. NORM-E: normoxicendotoxemia, HYPER-E: hyperoxic endotoxemia, HYPER: hyperoxia.
Mentions: During the hyperoxic/normoxic period, mean PaO2 was similar in thehyperoxia group and hyperoxic endotoxemia group(54.8 ± 3.0(411.7 ± 22.8) and54.1 ± 4.1(405.9 ± 31.1) kPa (mmHg),p = 0.89), whereas PaO2 in the hyperoxicendotoxemia group was higher than in the normoxic endotoxemia group(15.2 ± 0.7(114.3 ± 5.5) kPa,p < 0.0001, Fig. 2a).PaCO2 was 5.0 ± 0.3(37.8 ± 1.9) kPa in the hyperoxia group,5.5 ± 0.2(40.9 ± 1.2) kPa in the hyperoxicendotoxemia group, and 5.3 ± 0.2(39.5 ± 1.7) kPa in the normoxicendotoxemia group (Fig. 2b). After an initialincrease, PaCO2 decreased over time in the hyperoxia group. Asimilar pattern was observed in the normoxic endotoxemia and hyperoxicendotoxemia groups, with no differences between these groups (Fig. 2b). Lactate levels were in the normal range(<2 mmol/L) throughout the experiment in all subjects. Inall groups, mean arterial pressure (MAP) decreased over time, with nodifference between the normoxic and hyperoxic endotoxemia groups (Fig. 2c).

Bottom Line: Here, we demonstrate that, in the absence of systemic inflammation, short-term hyperoxia (100% O2 for 2.5 hours in mice and 3.5 hours in humans) does not result in increased levels of inflammatory cytokines in both mice and healthy volunteers.Furthermore, we show that, compared with room air, hyperoxia does not affect the systemic inflammatory response elicited by administration of bacterial endotoxin in mice and man.Our results indicate that hyperoxia does not exert direct anti-inflammatory effects and temper expectations of using it as an immunomodulatory treatment strategy.

View Article: PubMed Central - PubMed

Affiliation: Department of Intensive Care Medicine, Radboud university medical center, Geert Grooteplein Zuid 10, Nijmegen, 6500 HB, Netherlands.

ABSTRACT
Oxygen therapy to maintain tissue oxygenation is one of the cornerstones of critical care. Therefore, hyperoxia is often encountered in critically ill patients. Epidemiologic studies have demonstrated that hyperoxia may affect outcome, although mechanisms are unclear. Immunologic effects might be involved, as hyperoxia was shown to attenuate inflammation and organ damage in preclinical models. However, it remains unclear whether these observations can be ascribed to direct immunosuppressive effects of hyperoxia or to preserved tissue oxygenation. In contrast to these putative anti-inflammatory effects, hyperoxia may elicit an inflammatory response and organ damage in itself, known as oxygen toxicity. Here, we demonstrate that, in the absence of systemic inflammation, short-term hyperoxia (100% O2 for 2.5 hours in mice and 3.5 hours in humans) does not result in increased levels of inflammatory cytokines in both mice and healthy volunteers. Furthermore, we show that, compared with room air, hyperoxia does not affect the systemic inflammatory response elicited by administration of bacterial endotoxin in mice and man. Finally, neutrophil phagocytosis and ROS generation are unaffected by short-term hyperoxia. Our results indicate that hyperoxia does not exert direct anti-inflammatory effects and temper expectations of using it as an immunomodulatory treatment strategy.

No MeSH data available.


Related in: MedlinePlus