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目的 观察肝硬化内脏血管一氧化氮台酶（ＮＯＳ）表达及活性的动静脉差异在门静脉高压形成机制中的意义。方法 以四氯化碳皮下注射制备大鼠门静脉高压模型，应用免疫组织化学、化学发光以及ＲＴ－ＰＣＲ分别检测大鼠门静脉（ＰＶ）和肠系膜动脉（ＭＡ）组织ＮＯＳ的分布、活性及基因表达。结果 肝硬化组大鼠ＰＶ和ＭＡ血管各层均有ｉＮＯＳ分布，而ｅＮＯＳ则局限于内皮层。肝硬化大鼠内脏血管ＮＯＳ活性［ｐｍｏｌ·ｍｉｎ~(－１)·ｍｇ~(－１)·蛋白（ＰＶ ２３．８２±２．４８，ＭＡ ４３．４６±４．９３）］ 及ｍＲＮＡ表达均较对照组（ＰＶ １６．４８±１．５４，ＭＡ １６．９５±２．３４）显著升高（Ｐ＜０．０５与０．０１）；同时肝硬化大鼠ＭＡ的总ＮＯＳ活性和ｅＮＯＳ活性及ｅＮＯＳ ｍＲＮＡ表达均显著高于ＰＶ（Ｐ＜０．０１）。结论 内脏血管ｅＮＯＳ亚型活性及表达增加可能在肝硬化时ＮＯ产生增多中起主要作用，而ＮＯＳ活性及表达在ＭＡ与ＰＶ之间的动静脉差异，可能是ＮＯ参与门脉高压形成的重要机制之一．
Objective To observe the significance of arteriovenous differences in the expression and activity of nitric oxide synthase (NOS) in portal hypertension in cirrhotic patients with portal hypertension. Methods The rat portal hypertension model was induced by subcutaneous injection of carbon tetrachloride. The distribution, activity and gene expression of NOS in the portal vein (PV) and mesenteric artery (MA) were detected by immunohistochemistry, chemiluminescence and RT-PCR. Results There was iNOS distribution in PV and MA blood vessels in cirrhotic rats, while eNOS was confined to endothelial cells. The activity of NOS in the hepatic cirrhosis rats [pmol · min -1 (mg · -1) · protein (PV 23.82 ± 2.48, MA 43.46 ± 4.93)] and mRNA expression Compared with the control group (PV 16.48 ± 1.54, MA 16.95 ± 2.34) (P <0.05 and 0.01); at the same time, the total NOS activity and eNOS activity of MA in cirrhotic rats And eNOS mRNA expression were significantly higher than PV (P <0.01). Conclusions The increased activity and expression of eNOS in the visceral blood vessels may play a major role in the increase of NO production during cirrhosis. However, the difference in arteriovenous NOS activity and expression between MA and PV may be an important mechanism by which NO participates in the formation of portal hypertension one.