Hydrogen Water Reduces Lung Blood Pressure in Animal Study
- Authors
- Yasuaki Kishimoto, Taichi Kato, Mikako Ito, Yoshiteru Azuma, Yoshie Fukasawa, Kinji Ohno, Seiji Kojima
- Journal
- The Journal of Thoracic and Cardiovascular Surgery
- Year
- 2015
- DOI
- 10.1016/j.jtcvs.2015.05.052
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Pulmonary Arterial Hypertension
- Body System
- Cardiovascular
TL;DR
Drinking hydrogen-rich water reduced lung blood pressure and damage in rats with a condition similar to human high blood pressure in the lungs.
Key Finding
In rats with induced pulmonary arterial hypertension, hydrogen-saturated water significantly improved lung blood vessel function and reduced markers of inflammation and oxidative damage compared to control water.
Summary
Researchers gave rats a disease that damages blood vessels in the lungs (pulmonary arterial hypertension) and tested whether hydrogen-saturated water could help. Rats that drank hydrogen water showed significant improvement in their lung blood vessel function and had less inflammation and oxidative stress (cellular damage from harmful molecules) compared to rats that didn't receive hydrogen. The hydrogen appeared to work by reducing immune cell buildup and blocking certain inflammatory pathways.
Practical Takeaway
This is an early-stage animal study suggesting hydrogen water may help with pulmonary hypertension through anti-inflammatory and antioxidant mechanisms. However, results in rats do not automatically translate to humans, and no human trials have tested this approach. Anyone with pulmonary hypertension should consult their doctor before considering hydrogen water as a complementary approach.
Abstract
Objective: The pathogenesis of pulmonary arterial hypertension (PAH) involves reactive oxygen species and inflammation. Beneficial effects of molecular hydrogen, which exerts both anti-inflammatory and antioxidative effects, have been reported for various pathologic conditions. We therefore hypothesized that molecular hydrogen would improve monocrotaline (MCT)-induced PAH in rats. Methods: Nineteen male Sprague-Dawley rats (body weight: 200-300 g) were divided into groups, receiving: (1) MCT + hydrogen-saturated water (group H); (2) MCT + dehydrogenized water (group M); or (3) saline + dehydrogenized water (group C). Sixteen days after substance administration, we evaluated hemodynamics, harvested the lungs and heart, and performed morphometric analysis of the pulmonary vasculature. Macrophage infiltration, antiproliferating cell nuclear antigen-positive cells, 8-hydroxy-deoxyguanosine (8-OHdG)-positive cells, and expressions of phosphorylated signal transducers and activators of transcription-3 (STAT3) and nuclear factor of activated T-cells (NFAT) were evaluated immunohistochemically. Stromal cell-derived factor-1 and monocyte chemoattractant protein-1 expressions were evaluated by quantitative reverse-transcription polymerase chain reaction. Results: Pulmonary arterial hypertension was significantly exacerbated in group M compared to group C, but was significantly improved in group H. Vascular density was significantly reduced in group M, but not in group H. Adventitial macrophages, antiproliferating cell nuclear antigen - and 8-OHdG-positive cells, and stromal cell-derived factor-1 and monocyte chemoattractant protein-1 expressions were significantly increased in group M, but improved in group H. Expressions of phosphorylated STAT3 and NFAT were up-regulated in group M, but improved in group H. Conclusions: Molecular hydrogen ameliorates MCT-induced PAH in rats by suppressing macrophage accumulation, reducing oxidative stress and modulating the STAT3/NFAT axis.