门静脉高压症大鼠内毒素血症与一氧化氮变化

Endotoxemia and Alterations of Plasma Level of Nitric Oxide in Portal Hypertensive Rats

本研究拟通过测定门脉高压大鼠血浆内毒素和亚硝酸根/硝酸根离子(NO_2^-/NO_3^-)浓度,探讨一氧化氮(NO)在鼠门高压时产生是否过多及其可能机制.雌性SD大鼠分为三组:端侧门腔分流(PCS,n=10),门静脉部分缩窄引起的肝前型门高压(PHT,n=10)和手术对照组(Sham,n=8).模型制备后两周测定门脉压(FPP)并从腹主动脉采集血样,用于测定(1)血浆亚硝酸根/硝酸根离子浓度;(2)血浆内毒素浓度;(3)肝、肾功能.结果显示:血浆内毒素和NO_2^-/NO_3^-水平是PCS>PHT>Sham,且血浆内毒素与NO_2^-/NO_3^-之间呈密切正相关,提示门脉高压时因门体分流和肝功能减退导致血浆内毒素水平升高,刺激NO合成与释放增多.

The purpose of the present study is to evaluate whether there is over-production of nitric oxide in portal hypertensive rats and to elucide its mechanism. Twenty-eight female Sprague-Dawley rats were divided into three groups: end-to-side portacaval shunt (PCS, n=10), prehepatic portal hypertension by stenosis of the portal vein (PHT, n=10), and Sham-operated controls (SO, n=8). Two weeks after surgery, free portal pressure (FPP) was measured and blood samples from the abdominal aorta were obtained to measure: (1) the level of plasma nitrite (NO2-)/nitrate (NO3-); (2)the level of plasma endotoxin; (3) the liver and kidney functions. The results demonstrated that concentrations of plasma endotoxin and of plasma NO2-/NO3- were in the order of PCS>PHT>SO. Furthermore, a close positive correlation existed between plasma endotoxin and plasma NO2-/NO3-. The results suggested that both portosystemic shunting and liver dysfunction in portal hypertension resulted in increased concentration of plasma endotoxin, which caused increased NO production and release.