Research On Construction Of Pulmonary Artery Banding Model And The Mode Of Right Ventricular Remodeling In Neonatal Rats

Cardiovascular disease is the most common cause of death worldwide.One key issue to treat cardiovascular diseases is to prevent or reverse maladaptive ventricular remodeling that inevitably leads to heart failure.Mammalian cardiomyocytes are traditionally viewed as being permanently withdrawn from cell cycle and can't reproduce themselves to respond to various pathological stimuli.Therefore,cardiomyocyte hypertrophy and cardiac fibrosis are the major cellular remodeling to fulfill the functional compensation in adult mammalian heart.Recent studies reveal that mammalian heart can regenerate by cardiomyocyte proliferation within 1 week after birth in response to physical or ischemic lesions.In clinic,the most common pathological stimulus to neonatal heart is ventricular overload caused by anatomic defects and/or deformity.It would be interesting to know whether neonatal cardiomyocytes respond to ventricular overload by myocardial proliferation or cardiomyocyte hypertrophy and fibrosis which was the feature of adult mammalian ventricular remodeling.The core objective of this study is to explore the mode of ventricular remodeling respond to ventricular overload in newborn mammals.Here we generated the first neonatal right ventricle overload model by constricting pulmonary artery within 6hours after birth.Finally,we examined the proliferation,hypertrophy,apoptosis of cardiomyocytes and myocardial fibrosis at different time after operation to clarify the mode of ventricular remodeling caused by ventricular overload in newborn mammals.The results showed that the right ventricular hypertrophy caused by pulmonary artery banding in neonates was characterized by significantly cardiomyocyte proliferation and cardiomyocyte hypertrophy,but not accompanied by increased myocardial fibrosis and cardiomyocyte apoptosis.