Establishment and validation of acute myocardial injury model in mice with hypobaric hypoxia at extreme altitude

Abstract

Abstract Objective: To establish a novel mouse model of acute myocardial injury induced by hypobaric hypoxia and improve the relevant evaluation system. Methods: Using the plateau simulator made by our institute (which has e Chinese invention patent, patent number: ZL 2021 1 1517241. X), Babl/c mice were continuously exposed to the extreme altitude, low pressure and hypoxia environment for 0h-216h. PET/CT was used to evaluate the metabolic function of myocardial cells in mice by injecting 18F-FDG in vivo. the changes of cardiac function and morphology was observed in mice by cardiac ultrasound. FITC-BSA was injected into the tail vein to verify the leakage function of blood vessels in the heart tissue of mice. HE staining, Masson staining, CD163 and CD34 immunohistochemical staining get used to verify the degree of myocardial injury, fibrosis, inflammatory cell infiltration and angiogenesis in mice. Results: The myocardial metabolic function of Babl/c mice in hypobaric hypoxia environment was enhanced at the early stage of exposure, and then gradually weakened. With the extension of time, the heart rate gradually accelerated, the myocardial morphology changed significantly, the myocardial pathological changes and damage gradually increased, the role of vascular leakage gradually increased, the infiltration of inflammatory cells increased, and the myocardial fibrosis increased significantly.