Effect of Hyperbaric Oxygenation on the Severity of Experimental Autoimmune Myocarditis in Gal-3 Deficient Mice

Abstract Myocarditis is an inflammatory heart disease, which is characterized by the presence of a cellular infiltrate in the myocardial interstitium, along with the degeneration and necrosis of cardiomyocytes. Depending on the predominate immune mechanism in the disease, Gal-3 may either attenuate or enhance the development of inflammation. Treatment with hyperbaric oxygenation (HBO) is considered a promising adjunctive therapy for cardiovascular disease due to increasing evidence of its beneficial effect on myocardial function. The potential effects of HBO treatment on myocarditis in animal models have not been investigated. The aim of this study was to delineate the impact of HBO on both the clinical course and histochemical characteristics of EAM. EAM was induced in Gal-3-deficient mice on the C57BL/6J background by immunization with myosin peptide MyHCα 334–352 . The EAM group treated with HBO characteristically showed a significant improvement in FS compared to the untreated EAM group, as well as a reduction in LVIDd and LVIDs. Gal-3KO mice developed more severe myocarditis, characterized by accumulation of mononuclear cells and single mononuclear cells between cardiomyocytes, than animals treated with HBO. Additionally, EAM mice receiving HBO treatment showed a lower degree of degeneration and necrosis compared to the untreated EAM group. A significant reduction in fibrosis was noted in Gal-3KO mice with EAM after HBO treatment compared to the untreated group of EAM mice. The results showed that HBO treatment can improve cardiac function, reduce cardiac inflammatory infiltration, myocardial necrosis, and fibrosis, which could alleviate cardiac remodeling, dilated cardiomyopathy, and subsequent development of heart failure.