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Surgery. 2015 Aug;158(2):399-407. doi: 10.1016/j.surg.2015.03.038. Epub 2015 May 14.

Hydrogen inhalation protects against acute lung injury induced by hemorrhagic shock and resuscitation.

Author information

1
Department of Emergency, Disaster and Critical Care Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
2
Kobe University Graduate School of Health Science, Kobe, Hyogo, Japan.
3
Faculty of Health and Welfare Science, Okayama Prefectural University, Okayama, Japan.
4
Department of Surgery, University of Pittsburgh, Pittsburgh, PA.
5
Department of Emergency, Disaster and Critical Care Medicine, Hyogo College of Medicine, Nishinomiya, Japan. Electronic address: qq-nakao@hyo-med.ac.jp.

Abstract

INTRODUCTION:

Hemorrhagic shock followed by fluid resuscitation (HS/R) triggers an inflammatory response and causes pulmonary inflammation that can lead to acute lung injury (ALI). Hydrogen, a therapeutic gas, has potent cytoprotective, antiinflammatory, and antioxidant effects. This study examined the effects of inhaled hydrogen on ALI caused by HS/R.

METHODS:

Rats were subjected to hemorrhagic shock by withdrawing blood to lower blood pressure followed by resuscitation with shed blood and saline to restore blood pressure. After HS/R, the rats were maintained in a control gas of similar composition to room air or exposed to 1.3% hydrogen.

RESULTS:

HS/R induced ALI, as demonstrated by significantly impaired gas exchange, congestion, edema, cellular infiltration, and hemorrhage in the lungs. Hydrogen inhalation mitigated lung injury after HS/R, as indicated by significantly improved gas exchange and reduced cellular infiltration and hemorrhage. Hydrogen inhalation did not affect hemodynamic status during HS/R. Exposure to 1.3% hydrogen significantly attenuated the upregulation of the messenger RNAs for several proinflammatory mediators induced by HS/R. Lipid peroxidation was reduced significantly in the presence of hydrogen, indicating antioxidant effects.

CONCLUSION:

Hydrogen, administered through inhalation, may exert potent therapeutic effects against ALI induced by HS/R and attenuate the activation of inflammatory cascades.

PMID:
25983276
DOI:
10.1016/j.surg.2015.03.038
[Indexed for MEDLINE]

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