Effects Of The Components Of HuangQiDanshen Compound Prescription On Pregnant Rat Models Maded By Blocking Nitrogen Monoxide Synthesis

Objective: To investigate the potential curative mechanism of increasing the placental blood of the components in HuangQiDanShen compound prescription based on Qi-tonifying and bloodstasis-resolving therapy (YiQiHuaYu) in TCM.Methods: Effective components of astragalus root and red sage root were abstracted and made into injection(named "QIDAN injection").NOS blocker L-NANE was used to make PIH animal model on the 10th pregnant day, and nitroglycerin and the QIDAN injection were administered synchronously.Results: By inhibiting the synthesis of NO hypertension, albuminuria and some other PIH-related symptoms occurred in the pregnant rats ,and the rats of intrauterine growth retardation(IUGR) and fetal death in the uterus increased obviously. YiQiHuaYu therapy improved all measured growth parameters of fetus. The incidence of IUGR and fetal death in uterus decreased remarkably in the treatment group. YiQiHuaYu therapy decreased the levels of urine protein and blood pressure in pregnant model rats. YiQiHuaYu therapy improved uterine and placental circulation by regulating the endothelial cells function of secreting NO. YiQiHuaYu therapy protected the vascular endothelial cells by decreasing the level of cytotoxin TNFa. YiQiHuaYu therapy alleviated the congestion and inflammation of the uterus and placenta, protected the vascular endothelial cells from injury and facilitatethe restoring of the uterine and placental vessels.Conclusion: The results show that NO synthetical deficiency is an important factor or process in the pathogenesis of PIH. QIDAN injection based on the YiQiHuaYu therapy can improve the uterine and placental circulation by effecting the levels of NO and TNF, promoting the trophoblastic cell's growth and development and accelerating the process of placental revascularization. In a word, the results suggest that this prescription has a satisfactory curative effect on the placental blood deficiency induced by inhibiting NO synthesis.