Background: Hemorrhagic shock and resuscitation (HSR) is known to cause inflammatory reactions in the lung parenchyma and acute lung injury, increasing the risk of complications that can lead to death. Hydrogen gas has shown to inhibit the formation and eliminate reactive oxygen species (ROS), which are known to cause reperfusion injury. Hence, the purpose of this study was to investigate the protective effect of 2% inhaled hydrogen gas on post-HSR lung injury. Methods: Rats weighing 300–500 g were divided into three groups: sham, HSR, and hydrogen (H2)/HSR groups. In the latter two groups, HSR was induced via femoral vein cannulation. Gas containing 2% hydrogen gas was inhaled only by those in the H2/HSR group. Lung tissue and abdominal aorta blood were obtained for histologic examination and arterial blood gas analyses, respectively. Neutrophil infiltration and proinflammatory mediators were also measured. Results: PO2 was lower in the HSR and H2/HSR groups than in the sham group. Blood lactate level was not significantly different between the sham and H2/HSR groups, but it was significantly higher in the HSR group. Infiltration of inflammatory cells into the lung tissues was more frequent in the HSR group. Myeloperoxidase (MPO) activity was significantly different among the three groups (highest in the HSR group). All proinflammatory mediators, except IL-6, showed a significant difference among the three groups (highest in the HSR group). Conclusions: Inhalation of 2% hydrogen gas after HSR minimized the extent of lung injury by decreasing MPO activity and reducing infiltration of inflammatory cells into lung tissue.
- Hemorrhagic shock and resuscitation (HSR)
- Hydrogen gas
- Lung injury
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine