Molecular hydrogen reduces mean and systolic blood pressure in various forms of hypertension, as well as inflammatory processes in lung tissue, in Wistar rats

Molecular hydrogen demonstrates antioxidant and anti-inflammatory properties. It has been shown to have a protective effect in several cardiovascular diseases. The aim of this work was to study the effect of breathing atmospheric air containing 4% hydrogen on the degree of development of monocrotaline-induced pulmonary hypertension and associated lung tissue inflammation, as well as the severity of renovascular hypertension in Wistar rats. Methods. Monocrotaline-induced pulmonary hypertension (MCT-PH) was used as a model of small circle hypertension. Three groups of animals were used in the experiment: "Control" – animals injected with monocrotaline solvent, "MCT-Control" and "MCT-H2" – groups injected with MCT once. The "Control" and "MCT-Control" groups breathed atmospheric air for 21 days, and the "MCT-H2" group breathed air containing 4% hydrogen. Inhalations were kept constant until 21 days. On day 21, haemodynamic parameters were measured under urethane anesthesia and lung samples were fixed for subsequent morphological analysis. Renovascular hypertension 1R1С (RVH) was used as a model of systemic hypertension. There were two groups in the experiment: RVH-C – rats breathed atmospheric air and RVH-H2 rats breathed air containing 4% hydrogen. During the experiment, systolic blood pressure (SBP) was measured and renal excretory function was assessed. On day 28, haemodynamic parameters were measured under urethane anesthesia. Results. In the MCT model, hydrogen had no effect on the haemodynamic symptoms of MCT hypertension, but decreased mean blood pressure (MBP), SBP and the measured markers of connective tissue remodeling in the lungs, TGF-β and MMP-9, and resulted in decreased tryptase secretion and mast cell counts. In the RVG model, hydrogen breathing decreased MBP, SBP and had no effect on renal excretory function. Conclusion. Inhalation of 4% hydrogen reduces systemic MBP and SBP in both models of arterial hypertension, reduces the severity of the inflammatory process, regulates the phenotypic and functional status of mast cells and inhibits the activity of profibrotic factors in lung tissue in MCT-PH. It is likely that the central action of hydrogen is combined with its anti-inflammatory and anti-fibrotic effects.