Yanli Wang

To explore the efficacy and safety of prophylactic temporary balloon occlusion of the infrarenal abdominal aorta during caesarean for the management of patients with placenta praevia accreta. Two hundred and sixty-eight cases of placenta praevia accreta from January 2012 to June 2015 were retrospectively reviewed. Group A included two hundred and thirty patients who underwent prophylactic temporary balloon occlusion of infrarenal abdominal aorta followed by caesarean section. Group B included thirty-eight patients who underwent caesarean without endovascular intervention. The parameters including operating room time, estimated blood loss, blood transfusion volume, PT (prothrombin time) during operation, days in the intensive care unit, and total hospital days were compared between the two groups. The operating room time, estimated blood loss, PT, the incidence of hysterectomy, blood transfusion volume, postpartum haemorrhage, and days in intensive care unit were lower in group A than in group B, with statistical significance (P < 0.05). There was no significant difference in the Apgar scores of the neonates and the incidences of thrombosis in lower limbs between the two groups (P > 0.05). No patient in the group with prophylactic temporary balloon occlusion of the infrarenal abdominal aorta was performed hysterectomy, while three patients in group B were performed hysterectomy because of uncontrollable haemorrhage. The results indicate that prophylactic temporary balloon occlusion of infrarenal abdominal aorta followed by caesarean section is safe and effective to control intraoperative blood loss and greatly decreases the risk of hysterectomy in patients with placenta praevia accreta.

Pulmonary arterial hypertension (PAH) characterized by pulmonary vascular remodeling is a lethal disease. Paeoniflorin (PF) is a monoterpene glycoside with numerous beneficial functions, such as vasodilation, anti-inflammation and immunomodulation. This study aims to investigate the effects of PF on monocrotaline (MCT)-induced PAH rats. Our data showed that both prophylactic or therapeutic administration of PF alleviated MCT-induced increasing of right ventricular systolic pressure (RVSP), prevented right ventricle hypertrophy and pulmonary arterial remodeling, as well as inhibited inflammatory cell infiltration around pulmonary arteries. Meanwhile, PF blocked MCT-induced endothelial-mesenchymal transition (EndMT) as indicated by the restored expression of endothelial markers in lung. Moreover, PF inhibited MCT-induced down-regulation of bone morphogenetic protein receptor 2 (BMPR2) and suppressed MCT-induced phosphorylation of transforming growth factor- (TGF) activated kinase 1 (TAK1) in vivo. In vitro studies indicated that PF prevented human pulmonary arterial smooth muscle cells (PASMCs) from platelet-derived growth factor-BB (PDGF-BB)-stimulated proliferation and migration. PF also partially reversed TGF1, interleukin-1 (IL-1) and tumor necrosis factor (TNF-) co-stimulated endothelial-to-mesenchymal transition (EndMT) in cultured human pulmonary artery endothelial cells (HPAECs). Signaling pathway analysis demonstrated that the underlying mechanism might be associated with the inhibition of TAK1-MAPK/NF-B pathways. Taken together, our results suggested that PF could be a potential drug for the treatment of PAH.