Objective: To explore the mechanism by which mechanical ventilation improves myocardial injury in rats with acute heart failure (AHF).
Methods: Thirty-six male Sprague Dawley rats were randomized into a sham group, heart failure (HF) group, and mechanical ventilation (MV) group. The AHF rat model was established by pentobarbital perfusion under right internal jugular vein monitoring. The symptoms of heart failure, changes in hemodynamic parameters, cardiac function, N-terminal pro-B-type natriuretic peptide (NT-proBNP), oxidative stress-related indicators, myocardial apoptosis index, and expression of apoptosis-related proteins were compared in an AHF rat model with or without mechanical ventilation.
Results: Compared to the sham group, the hemodynamics and cardiac function of MV and HF groups were markedly reduced (P<0.05), and the serum levels of NT-proBNP of MV and HF groups were elevated (P<0.05). The levels of malondialdehyde (MDA) were lowest in the sham group, followed by the MV group, and highest in the HF group. Glutathione (GSH) and superoxide dismutase (SOD) were lowest in the HF group, inermediate in MV group, and highest in the sham group (P<0.05). Mechanical ventilation improved myocardial injury and reduced apoptosis of myocardial cells in a rat model of AHF.
Conclusion: Mechanical ventilation in the early stage of heart failure can significantly reduce the excessive occurrence of oxidative stress in rats and significantly improve apoptosis in myocardial cells in AHF rats, so as to effectively improve the symptoms of AHF and reduce the mortality of AHF rats.
Keywords: Acute heart failure; apoptotic cardiomyocytes; mechanical ventilation; oxidative stress.
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