Hydrogen Water Prevents Blood Clots in Animal Study

Authors
Journal
Life Sciences
Year
DOI
10.1016/j.lfs.2019.116700
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Thrombosis
Body System
Cardiovascular

TL;DR

Hydrogen-rich saline can prevent blood clots by reducing platelet activity and has potential as an antithrombotic treatment.

Key Finding

Hydrogen-rich saline inhibited platelet activation and reduced thrombus (blood clot) formation in both laboratory tests and animal models, suggesting potential antithrombotic effects.

Summary

Researchers tested whether hydrogen-rich saline (a solution with dissolved hydrogen gas) could prevent blood clots by studying how it affects platelets (blood cells that form clots). In lab tests and animal studies, hydrogen-rich saline slowed clot formation, reduced platelet clumping, and increased bleeding time. The researchers found that hydrogen appears to work by reducing harmful molecules called free radicals and activating a protective pathway in platelets that involves nitric oxide, a natural blood vessel relaxer.

Practical Takeaway

This animal study provides early evidence that hydrogen may help prevent blood clots through antioxidant mechanisms, but it is not yet clear whether these effects would translate to humans. Much more research, including human trials, would be needed before hydrogen water could be considered for clot prevention. Anyone concerned about thrombosis should consult their healthcare provider about proven preventive strategies.

Abstract

Aims: Hydrogen (H2) has antioxidant effects. The pharmacologic function of H2 in platelets is not yet clear. Therefore, in this study we sought to investigate the inhibitory effects of H2 on in vitro platelet activation and in vivo prevention of thrombus formation. Main methods: After platelets were incubated with H2-rich saline (HRS), platelet adhesion in whole human blood was assessed in fibrinogen-coated perfusion chambers, while rat platelet aggregation induced by ADP, collagen and H2O2 was detected through light transmission aggregometry. The level of P-selectin, thromboxane B2, nitric oxide (NO), malondialdehyde, reactive oxygen species (ROS), cGMP, extracellular signal-regulated kinases 1 and 2 (p-ERK1/2), and fibrinogen binding to platelets were evaluated in vitro. Besides, the in vivo effects were examined in arterio-venous shunt thrombosis, FeCl3-induced artery thrombus formation, and tail bleeding time in mice and rats. Key findings: HRS prolonged tail bleeding time in mice and rats, decreased thrombus weight and prolonged the time to occlusion in rat and mouse thrombosis models in vivo and inhibited platelet adhesion as well as aggregation in vitro. Additionally, HRS decreased P-selectin expression, release of thromboxane B2, ROS, and fibrinogen binding, but enhanced NO levels in H2O2-exposed platelets. HRS also decreased malondialdehyde levels in plasma of the rat arterial thrombosis or H2O2-exposed platelet model. Moreover, HRS increased cGMP level, decreased p-ERK1/2 (diminished with KT5823) in the platelets stimulated by H2O2. Significance: These results suggest that H2 has antithrombotic effects, which may be due to its antioxidant property and subsequent inhibition of platelet activation via NO/cGMP/PKG/ERK pathway.