Hydrogen gas inhalation ameliorates lung injury after hemorrhagic shock and resuscitation

Duk Hwan Moon, Du Young Kang, Seok Jin Haam, Tetsuya Yumoto, Kohei Tsukahara, Taihei Yamada, Atsunori Nakao, Sungsoo Lee

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish
Pages (from-to)1519-1527
Number of pages9
JournalJournal of Thoracic Disease
Volume11
Issue number4
DOIs
Publication statusPublished - Apr 1 2019

Fingerprint

Hemorrhagic Shock
Lung Injury
Resuscitation
Inhalation
Hydrogen
Gases
Lung
Peroxidase
Blood Gas Analysis
Femoral Vein
Neutrophil Infiltration
Acute Lung Injury
Abdominal Aorta
Adult Respiratory Distress Syndrome
Reperfusion Injury
Catheterization
Lactic Acid
Interleukin-6
Reactive Oxygen Species

Keywords

  • Hemorrhagic shock and resuscitation (HSR)
  • Hydrogen gas
  • Lung injury

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Hydrogen gas inhalation ameliorates lung injury after hemorrhagic shock and resuscitation. / Moon, Duk Hwan; Kang, Du Young; Haam, Seok Jin; Yumoto, Tetsuya; Tsukahara, Kohei; Yamada, Taihei; Nakao, Atsunori; Lee, Sungsoo.

In: Journal of Thoracic Disease, Vol. 11, No. 4, 01.04.2019, p. 1519-1527.

Research output: Contribution to journalArticle

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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

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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.

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