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-inflammatoryproperties. It has been shown to have a protective effect in severalcardiovascular diseases. The aim of this work was to investigatethe effect of breathing atmospheric air containing 4% hydrogen onthe degree of development of monocrotaline-induced pulmonary hypertensionand associated lung tissue inflammation, as well as the degree ofrenovascular hypertension in Wistar rats. Monocrotaline-inducedpulmonary hypertension (MCT-PH) was used as a model of pulmonarycirculation hypertension. Three groups of animals were used in theexperiment: “Control”—animals injected with monocrotaline solvent,“MCT-Control” and “MCT-H₂”—groups injectedwith MCT once. The “Control” and “MCT-Control” groups breathed atmosphericair for 21 days, and the “MCT-H₂” group breathedair containing 4% hydrogen. The inhalations were kept constant until21 days. On day 21, haemodynamic parameters were measured underurethane anesthesia and lung samples were fixed for subsequent morphologicalanalysis. Renovascular hypertension 1R1C (RVH) was used as a modelof systemic hypertension. There were two groups in the experiment:RVH-C—rats breathed atmospheric air and RVH-H₂ ratsbreathed air containing 4% hydrogen. During the experiment, systolicblood pressure (SBP) was measured and renal excretory function wasassessed. On day 28, haemodynamic parameters were measured underurethane anesthesia. In the MCT model, hydrogen had no effect onthe haemodynamic symptoms of MCT hypertension, but decreased meanblood pressure (MBP), SBP and the measured markers of connective tissueremodeling in the lungs, TGF-β1 and MMP-9, and resulted in decreasedtryptase secretion and mast cell counts. In the RVG model, hydrogenbreathing decreased MBP, SBP and had no effect on renal excretoryfunction. Inhalation of 4% hydrogen reduces systemic MBP and SBPin both models of arterial hypertension, reduces the severity ofthe inflammatory process, regulates the phenotypic and functionalstatus of mast cells and inhibits the activity of profibrotic factorsin lung tissue in MCT-PH. It is likely that the central action ofhydrogen is combined with its anti-inflammatory and anti-fibrotic effects.