Hydrogen Gas Inhalation Protects Lungs After Blood Loss and Resuscitation
- Authors
- Duk Hwan Moon, Du-Young Kang, Seok Jin Haam, Tetsuya Yumoto, Kohei Tsukahara, Taihei Yamada, Atsunori Nakao, Sungsoo Lee
- Journal
- Journal of Thoracic Disease
- Year
- 2019
- DOI
- 10.21037/jtd.2019.03.23
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- South Korea
- Health Condition
- Hemorrhagic Shock
- Body System
- Respiratory
TL;DR
Breathing in 2% hydrogen gas helped reduce lung damage in rats after a simulated blood loss and resuscitation event.
Key Finding
Rats that inhaled 2% hydrogen gas after hemorrhagic shock and resuscitation showed significantly reduced lung inflammation and fewer inflammatory cells in lung tissue compared to untreated controls.
Summary
This study tested whether inhaled hydrogen gas could protect rat lungs from injury caused by severe bleeding and resuscitation. Researchers compared three groups of rats: a control group, a group that experienced bleeding/resuscitation without hydrogen, and a group that received 2% hydrogen gas after bleeding/resuscitation. The hydrogen-treated group showed less inflammation and fewer immune cells in lung tissue compared to the untreated bleeding group, suggesting hydrogen gas may reduce lung damage by neutralizing harmful molecules called reactive oxygen species.
Practical Takeaway
This is an early-stage animal study showing hydrogen gas inhalation may help protect lungs from injury related to severe blood loss and resuscitation. However, this was only tested in rats, and much more research—including human trials—would be needed before any conclusions could be drawn about potential benefits for people in critical care situations.
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 (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.