一氧化氮在孕鼠妊高征发病中的作用

Role of Nitric Oxide in Pathogenesis of Pregnancy Induced Hypertension

目的：探讨一氧化氮（ＮＯ）在大鼠妊高征发病中所起的作用。方法：用一氧化氮合成酶抑制剂Ｌ－ＮＡＭＥ抑制妊娠晚期大鼠（妊娠组）及未妊娠鼠（对照组）体内ＮＯ的合成，测定大鼠血压、尿蛋白、血小板（ＰＬＴ）、血红蛋白（ＨＧＢ）、红细胞压积（ＨＣＴ）、血浆内皮素（ＥＴ）、血栓素Ｂ２（ＴＸＢ２）、６－酮－前列腺素Ｆ１α（６－ｋｅｔｏ－ＰＧＦ１α）水平。同时测量足月新生鼠身长、体重、肝、脑、胎盘重量和观察胎盘组织结构变化。结果：抑制ＮＯ合成后，妊娠组大鼠血压升高，尿蛋白增加，ＰＬＴ减少，ＨＣＴ升高，ＥＴ升高，ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１α比值降低。与对照组比较，均有统计学意义。妊娠组新生鼠身长、体重、胎盘重均有显著变化。胎盘各层均有严重的缺血缺氧表现，血管可见微血栓及内皮细胞增生。结论：妊娠大鼠体内ＮＯ减少，会出现血管舒、缩因子平衡失调，导致妊高征发生。ＮＯ在妊高征发生和发展中起着关键的作用。

Objective: To investigate the role of nitric oxide (NO) in pathogenesis of pregnancy induced hypertension (PIH). Methods: N(G)nitroLargininemethylester (LNAME) was used to inhibite the synthesizing of NO in the third trimester of pregnancy rats. Indices including HGB, PLT, HCT, protein uria, serum endothelin (ET), thromboxane B2(TXB2), 6ketoPGF1α and blood pressure in pregnant rats were measured. The length, weight of body, liver and brain of fullterm newborn rats and the weight and pathological change of placenta were observed. Results: After inhibition of NO synthesis, blood pressure were consistently high. The protein uria, HCT, ET, TXB2/6ketoPGF1α were significantly higher and PLT was significantly lower than that of control group. The length, weight of body and placenta in neonatal rats were lower than those of the control group (P<0.01). Severe ischimic lesion, thrombosis of vessels and endothelial proliferation in placenta were observed. Conclusion: NO plays an important role in pathogenesis of PIH. 