TY - JOUR
T1 - Hydrogen gas inhalation ameliorates lung injury after hemorrhagic shock and resuscitation
AU - Moon, Duk Hwan
AU - Kang, Du Young
AU - Haam, Seok Jin
AU - Yumoto, Tetsuya
AU - Tsukahara, Kohei
AU - Yamada, Taihei
AU - Nakao, Atsunori
AU - Lee, Sungsoo
PY - 2019/4/1
Y1 - 2019/4/1
N2 -
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 (H
2
)/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 H
2
/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: PO
2
was lower in the HSR and H
2
/HSR groups than in the sham group. Blood lactate level was not significantly different between the sham and H
2
/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.
AB -
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 (H
2
)/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 H
2
/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: PO
2
was lower in the HSR and H
2
/HSR groups than in the sham group. Blood lactate level was not significantly different between the sham and H
2
/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.
KW - Hemorrhagic shock and resuscitation (HSR)
KW - Hydrogen gas
KW - Lung injury
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U2 - 10.21037/jtd.2019.03.23
DO - 10.21037/jtd.2019.03.23
M3 - Article
AN - SCOPUS:85065432404
VL - 11
SP - 1519
EP - 1527
JO - Journal of Thoracic Disease
JF - Journal of Thoracic Disease
SN - 2072-1439
IS - 4
ER -