Correlation between Platelet-Derived Growth Factor-BB and Pulmonary Vascular Remodeling in Neonatal Rats with Hypoxic Pulmonary Hypertension

Objective: To investigate the correlation between platelet-derived growth factor-BB (PDGF-BB) and hypoxia-inducible factor-1 alpha (HIP-1 alpha) in the proliferation of pulmonary artery smooth muscle cells (PASMCs) in neonatal rats with hypoxic pulmonary hypertension (HPH) and the effect of PDGF-BB on pulmonary vascular remodeling and right ventricular structure and function in this disease.Methods: Sixty-four neonatal rats were randomly divided into an HPH and control group. Based on the observation time points, each group was split into groups for days 3, 7, 14, and 21. The HPH model was established in the HPH group. After detecting right ventricular systolic pressure (RVSP) in the neonatal rats in each group at the corresponding observation time points, the rats were sacrificed to obtain heart and lung tissue samples. The pulmonary vascular remodeling indexes and right ventricular hypertrophy index (RVHI) were calculated. PDGF-BB, HIP-1 alpha, and proliferating cell nuclear antigen (PCNA) expression levels in the lung tissue were evaluated.Results: (1) The RVSP in the HPH group was higher than that in the control group at each observation time point (p < 0.001). (2) The pulmonary vascular remodeling indexes in the neonatal rats in the HPH group after 7 days of hypoxia were higher than those in the control group (p < 0.05). With the prolongation of hypoxia, the pulmonary vascular remodeling indexes gradually increased. (3) After hypoxia for 7, 14, and 21 days, the RVHI of the neonatal rats in the HPH group was significantly higher than that of the control group at the same age (p < 0.001). (4) PDGF-BB, HIP-1 alpha, and PCNA expression levels in the HPH group at each observation time point were higher than those in the control group (p < 0.05), gradually increasing with the prolongation of hypoxia.Conclusions: In HPH neonatal rats, PDGF-BB, HIP-1 alpha, and PCNA expression levels and the number of PASMCs are increased, which leads to pulmonary vascular remodeling and increased pulmonary artery pressure.