中文摘要：

目的探讨NO在肝硬化门静脉高压症血管收缩反应中发挥作用的机制，特别是NO与RhoA／ROCK通路问的相互作用机制。方法分别测定正常大鼠（正常对照组，5只）、CCl4诱导的肝硬化门静脉高压症大鼠（实验对照组，6只）和经L-NAME处理的门静脉高压症大鼠（L-NAME处理组，6只）外周血和肠系膜动脉NO含量；利用血管灌流系统测定上述3组大鼠肠系膜微动脉对去甲肾上腺素的反应；Westernblot分别检测3组大鼠肠系膜动脉NO-cGMP-PKG通路和RhoA／ROCK相关蛋白表达水平的变化。多组间均数比较采用单因素方差分析，两两比较采用LSD-t检验，肠系膜微动脉对去甲肾上腺素反应性的变化通过量．效曲线表示，运用非线性回归法，计算出EC50值。结果（1）正常对照组、实验对照组和L-NAME处理组大鼠平均门静脉压力分别为（6．2±0．9）mmHg（1mmHg=0．133kPa）、（13．9±1．7）mmHg和（16．6±1．3）mmHg，3组比较，差异有统计学意义（F=94．4，P〈0．05）。（2）正常对照组、实验对照组和L-NAME处理组大鼠平均血清NO浓度分别为（43±5）μmol／L、（82±16）μmol／L和（45±9）μmol／L，3组比较，差异有统计学意义（F=24．77，P〈0．05）；L-NAME处理组大鼠平均NO浓度明显低于实验对照组（P〈0．05）。（3）正常对照组、实验对照组和L-NAME处理组大鼠肠系膜动脉平均NO含量分别为（236±41）μmol／g、（407±82）μmol／g和（216±42）μmol／g，3组比较，差异有统计学意义（F=20．29，P〈0．05）；L-NAME处理组大鼠肠系膜动脉平均NO含量明显低于实验对照组（P〈0．05）。（4）与实验对照组大鼠比较，L-NAME处理组大鼠的离体肠系膜微动脉对去甲肾上腺素剂量反应曲线左移，但未达到正常对照组大鼠反应曲线水平，正常对照组、实验对照组和L-NAME处理组大鼠EC50分别为6．458×10-7mol、9．546×10-7mol和7．494×1

英文摘要：

Objective To investigate the mechanisms of nitric oxide （NO） in decreasing intestinal mesenterie arterial hypoeontraetility in rats with hepatic cirrhosis and portal hypertension, and to analyze the inter- action of NO and RhoA/ROCK pathway. Methods The levels of NO in the peripheral blood and mesenteric artery of normal rats （normal control group, 5 rats）, rats with portal hypertension （experimental control group, 6 rats） and rats with portal hypertension treated by L-NAME （L-NAME group, 6 rats） were detected. Mesenteric arteriolecontractility to norepinephrine in the 3 groups was determined using a vessel perfusion system. The expressions of proteins of NO-cGMP-PKG pathway and RhoA/ROCK pathway in the 3 groups were detected by Western blot. All data were analyzed using the analysis of variance or LSD-t test. The changes of mesenteric arteriole contractility to norepinephrine was expressed in dose-response curve, and was analyzed using the nonlinear regression method, and the ECso value was calculated. Results （ 1 ） The pressures of portal veins of the normal control group, exper- imental control group and L-NAME group were （6.2 ± 0.9）mm Hg （1 mm Hg = 0. 133 kPa）, （13.9 ± 1.7）mm Hg and （ 16.6 ± 1.3 ）mm Hg, respectively, with a significant difference among the 3 groups （ F = 94.4, P 〈 0.05 ）. （2） The levels of NO in the normal control group, experimental control group and L-NAME group were （43± 5）μmol/L, （ 82 ±16 ） μmol/L and （ 45 ± 9 ） μmol/L, respectively, with a significant difference among the 3 groups （F = 24. 77, P 〈 0.05 ）. The level of NO of the L-NAME group was significantly lower than that of the experimental control group （ P 〈 0.05 ）. （ 3 ） The levels of NO in the mesenteric artery of the normal control group, experimental control group and L-NAME group were （236 ± 41 ）μmol/g, （407 ± 82）μmol/g and （216 ± 42） μmol/g, respectively, with a significant difference among the 3 groups （ F = 20. 29, P 〈 0.