Hydrogen Gas Reduces Heart Problems in Pulmonary Hypertension Rats

Authors
Journal
Biomedicines
Year
DOI
10.3390/biomedicines14030494
Study Type
Rat
Outcome
Positive
Peer Reviewed
Yes
Country
Russia
Health Condition
Pulmonary Hypertension
Body System
Cardiovascular

TL;DR

Hydrogen inhalation reduced heart rate response to hypotension and decreased vascular reactivity in a rat model of pulmonary hypertension.

Key Finding

Rats with pulmonary hypertension that breathed hydrogen gas showed a 34% smaller heart rate response to blood pressure-lowering medication and 30% less blood vessel tightening to a stimulating drug compared to rats breathing regular air.

Summary

This study tested whether breathing hydrogen gas could help rats with pulmonary hypertension (high blood pressure in the lungs). Researchers gave some rats hydrogen gas to breathe for 2 hours twice daily over 21 days, while others breathed regular air. They then measured how the rats' hearts and blood vessels responded to certain drugs. Rats that breathed hydrogen showed smaller heart rate increases when their blood pressure dropped, and their blood vessels were less reactive to a drug that normally tightens them. The researchers also found signs of reduced inflammation in the hydrogen-treated rats.

Practical Takeaway

This early animal study suggests hydrogen gas inhalation may help modulate how the body controls blood pressure in pulmonary hypertension, but these results are from rats only and cannot yet be applied to humans. Much more research, including human trials, would be needed to determine if hydrogen therapy could be beneficial for people with this condition.

Abstract

Background/Objectives: Molecular hydrogen (H2), a natural antioxidant, can selectively reduce hydroxyl radicals and peroxynitrite without affecting signaling molecules such as H2O2 and NO. In addition, H2 can inhibit the synthesis of inflammatory cytokines. Human and animal studies have shown that the inhalation of H2 has a hypotensive effect. In this context, the aim of the present work was to study the effect of H2 on the baroreflex regulation of blood pressure in rats with experimental monocrotaline-induced pulmonary hypertension (MCT) in vivo and the effects of H2 on the reactivity of isolated rat aorta with MCT pulmonary hypertension to α1-adrenoceptor agonists in vitro. Methods: Experiments were performed on male Wistar rats with MCT pulmonary hypertension; animals were placed in plastic chambers aerated with atmospheric air at a rate of 4 L/min with O2 and CO2 control. Cages with the rats of the MCT-H2 and Control-H2 groups were ventilated with air containing 4% H2 twice daily for 2 h each. The MCT-Air and Control-Air groups breathed only atmospheric air. The duration of the experiment was 21 days. On day 20, blood pressure and heart rate (HR) were measured in awake animals and the baroreflex response to phenylephrine (PE) and nitroprusside (NP) was tested. In in vitro experiments, we studied the effect of adding H2 to the perfusion solution on the responsiveness of isolated aortic preparations from MCT and control rats to the α1-adrenoceptor agonist PE and the vasodilators NP and Acetylcholine. Results: When the effect of H2 on the baroreflex response to NP (4.5 μg/kg) was examined in awake rats, the increase in HR was 73.1 ± 16.7 beats/min in the MCT-Air group and 48.1 ± 10.2 beats/min in the MCT-H2 group (p 2 and Control-Air groups, there was a trend towards a lower HR in the Control-H2 group, but the differences were not significant. No differences in HR response to PE administration were found between any of the experimental groups. Experiments on isolated aortic preparations from MCT rats showed that the addition of H2 to the perfusion medium resulted in a 30% reduction in the maximal response to PE compared with the MCT group without hydrogen (p 50) decreased threefold (p 2. Conclusions. The results demonstrate that H2 inhalation was associated with an attenuated heart rate response to nitroprusside-induced hypotension and reduced vascular reactivity to phenylephrine in rats with pulmonary hypertension.