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Ideal concentrations of inhaled oxygen with regard to lung protection during early traumatic hemorrhagic shock (THS) remain unknown especially in the era of targeted temperature management (TTM). We speculated that a significant increase in oxygen supply in early stage of THS would magnify the protecting role of hypothermia in acute lung injury. Forty male New Zealand rabbits were randomly divided into four groups (n = 10): sham group, control group, group 1, and group 2. Except for sham group, all other animals were submitted to 30 min of uncontrolled THS and received limited fluid resuscitation for 60 min. During resuscitation, in addition to 34°C of TTM, animals in group 1 inhaled 21% oxygen while animals in group 2 inhaled 50% oxygen. Animals in control group inhaled room air and were kept normothermia. Oxidative stress, inflammation, and apoptosis parameters in the lung tissues were determined. THS induced higher expression of malondialdehyde, surfactant protein A, nuclear factor kappa B, and caspase 3 as well as lower expression of Bcl-2 mRNA and superoxide dismutase activity. Compared with inhalation of 21% oxygen, inhalation of 50% oxygen during TTM significantly improves oxidative stress, inflammation, apoptosis, and acute lung injury. Oxygen supplement during TTM therapy alleviated acute lung injury in the early stage of THS. Further studies are required to explore the ideal combination forms of TTM and oxygen supplement with the purpose of maximizing therapeutic effect while minimizing adverse effects. [ABSTRACT FROM AUTHOR]

Ideal concentrations of inhaled oxygen with regard to lung protection during early traumatic hemorrhagic shock (THS) remain unknown especially in the era of targeted temperature management (TTM). We speculated that a significant increase in oxygen supply in early stage of THS would magnify the protecting role of hypothermia in acute lung injury. Forty male New Zealand rabbits were randomly divided into four groups (n = 10): sham group, control group, group 1, and group 2. Except for sham group, all other animals were submitted to 30 min of uncontrolled THS and received limited fluid resuscitation for 60 min. During resuscitation, in addition to 34°C of TTM, animals in group 1 inhaled 21% oxygen while animals in group 2 inhaled 50% oxygen. Animals in control group inhaled room air and were kept normothermia. Oxidative stress, inflammation, and apoptosis parameters in the lung tissues were determined. THS induced higher expression of malondialdehyde, surfactant protein A, nuclear factor kappa B, and caspase 3 as well as lower expression of Bcl-2 mRNA and superoxide dismutase activity. Compared with inhalation of 21% oxygen, inhalation of 50% oxygen during TTM significantly improves oxidative stress, inflammation, apoptosis, and acute lung injury. Oxygen supplement during TTM therapy alleviated acute lung injury in the early stage of THS. Further studies are required to explore the ideal combination forms of TTM and oxygen supplement with the purpose of maximizing therapeutic effect while minimizing adverse effects. [ABSTRACT FROM AUTHOR]