一氧化氮在肝前性门静脉高压症形成中的作用

目的：了解一氧化氮（NO）在肝前性门静脉高压症形成中的作用。方法：部分门静脉结扎（PVL）法制备肝前性门静脉高压症大鼠模型，以硝酸还原酶和比色法检测正常组，假手术（SO）组及PVL组术后不同时间点的门静脉血浆NO、一氧化氮合酶（NOS）水平，观察其血流动力学指标的动态变化及NOS抑制剂硝基－L－精氨酸甲酯(L-NAME)对门静脉高压大鼠血流动力学的影响。结果：SO组各时间点与正常组比较，NO，NOS及血流动力学指标均无显性差异，PVL组术后各时间点与正常组比较，NO，NOS，门静脉压力（PVP），门静脉阻力（PVR）明显升高（P＜0．05），平均动脉压（MAP），内脏血管阻力（SVR）明显降低（P＜0．05），门静脉血流量（PVF）无显性差异，且血浆NO水平与PVP，PVF，SVR，MAP呈显相关性，NAME能使门静脉高压大鼠PVP，PVR显下降（P＜0．05），使SVR，MAP显上升（P＜0．05）。结论：门静脉高压症大鼠存在高动力循环状态；NO参与了PVL术后血流动力学的变化及肝前性门静脉高压症模型的形成。

Role of nitric oxide in pathogenesis of prehepatic portal hypertension

Objective: To ascertain the role of nitric oxide (NO) in the pathogenesis of prehepatic portal hypertension. Methods: The models of prehepatic portal hypertension were established in SD rats by means of partial portal vein ligation (PVL). The plasma levels of NO and nitric oxide synthase(NOS) in the portal veins were detected with nitric reductase and colorimetry. The rats were divided into normal, sham operation (SO) and PVL group. SO and PVL rats were divided into subgroups according to different time after operations. The changes of hemodynamic indexes in rats were measured; The effects of L-NG-nitro-arginine methyl ester (L-NAME) , an inhibitor of NO biosynthesis were investigated in portal hypertension rats. Results: NO and NOS levels and hemodynamic indexes after SO were not markedly different from those of normal groups. Significant increases were noted in NO, NOS levels and portal venous pressure (PVP), portal vascular resistance (PVR) at different time after PVL compared with normal controls(F<0. 05), whereas mean arterial pressure(MAP) and splanchnic vascular resistance(SVR) were significantly decreased(P<0. 05) and portal venous flow(PVF) was not markedly different from those of normal controls. In addition, the plasma NO levels were correlated with PVP, PVF, SVR and MAP. Administration of L-NAME significantly decreased PVP, PVR and increased SVR, MAP in portal hypertensive rats. Conclusion: The portal hypertensive rats are in hyperdynamic circulatory state. NO plays a key role in the hemodynamic changes of PVL rats and the induction of prehepatic portal hypertension.