Hydrogen Gas Protects Against Eye Damage From Blood Flow Loss in Rats
- Authors
- Mitsuya Otsuka, Kenichi Arai, Yoshiko Yoshida, Atsushi Hayashi
- Journal
- Graefe's Archive for Clinical and Experimental Ophthalmology
- Year
- 2023
- DOI
- 10.1007/s00417-023-06262-3
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Retinal Ischemia-Reperfusion Injury
- Body System
- Visual System
TL;DR
Breathing in hydrogen gas helps protect rats' eyes from damage caused by temporary loss and restoration of blood supply.
Key Finding
Inhaling 1.8% hydrogen gas significantly reduced retinal damage and inflammation in rats experiencing temporary loss of blood flow to the eye, preserving both the structure and function of the retina.
Summary
Researchers tested whether inhaling hydrogen gas could protect rat eyes from damage caused by temporarily cutting off blood flow and then restoring it (a condition called ischemia-reperfusion injury). Rats that inhaled 1.8% hydrogen gas during the blood flow interruption showed better preservation of retinal structure, less inflammation, and better visual function compared to rats that breathed regular air. The hydrogen-treated rats had thicker inner retinal layers, fewer inflammatory cells, and lower levels of inflammatory proteins.
Practical Takeaway
This rat study suggests hydrogen gas inhalation may help protect against vision loss from conditions involving reduced blood flow to the eye. However, this is early-stage animal research, and it remains unclear whether these results would translate to humans or what dose and delivery method would be appropriate. Further human studies would be needed before any therapeutic recommendations could be made.
Abstract
Purpose: To investigate the inhibitory effect of hydrogen gas inhalation on retinal ischemia reperfusion (I/R) injury using a rat model. Methods: Six-week-old male Sprague-Dawley rats were used. A 27G needle connected by a tube to a saline bottle placed 200 cm above the eye was inserted into the anterior eye chamber to create a rat retinal I/R model. In the ischemia-plus-hydrogen-gas group (H2( +) group), the ischemia time was set to 90 min, and 1.8% hydrogen was added to the air delivered by the anesthesia mask simultaneously with the start of ischemia. In the non-hydrogen-treatment ischemia group (H2( -) group), I/R injury was created similarly, but only air was inhaled. ERGs were measured; after removal of the eyes, the retina was examined for histological, immunostaining, and molecular biological analyses. Results: The mean thickness of the inner retinal layer in the H2( +) group was 107.2 ± 16.0 μm (n = 5), significantly greater than that in the H2( -) group (60.8 ± 6.7 μm). Immunostaining for Iba1 in the H2( -) group showed increased numbers of microglia and microglial infiltration into the subretinal space, while there was no increase in microglia in the H2( +) group. B-wave amplitudes in the H2( +) group were significantly higher than in the H2( -) group. In the membrane antibody array, levels of interleukin-6, monocyte chemotactic protein 1, and tumor necrosis factor alpha were significantly lower in the H2( +) group than in the H2( -) group. Conclusion: Inhalation of 1.8% hydrogen gas inhibited the induction of inflammation, morphological/structural changes, and glial cell increase caused by retinal I/R injury. Keywords: Cytokine; Hydrogen gas; Inhalation; Ischemia–reperfusion injury; Retina.