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目的探讨门脉高压症血管反应性变化与一氧化氮(NO)的关系.方法采用部分门静脉结扎大鼠为模型,研究加和不加一氧化氮合成酶抑制剂Nω硝基L精氨酸(NωnitroLarginine,LNNA)两种情况下,离体腹主动脉条对不同浓度的氯化钾(KCl)(10mmol/L~80mmol/L)和苯肾上腺素(109mol/L~104mol/L)的收缩反应性变化.结果KCl的EC50值(265mmol/L±09mmol/L)明显高于对照组(233mmol/L±17mmol/L,P<001),苯肾上腺素的EC50值(372nmol/L±04nmol/L)也显著高于对照组(286nmol/L±02nmol/L,P<001).显示部分门静脉结扎组大鼠腹主动脉对KCl和苯肾上腺素的收缩反应下降.应用LNNA后,门脉高压组和对照组KCl的EC50值分别为2118mmol/L±08mmol/L和194mmol/L±12mmol/L,二者相差不显著(P>005);KCl的最大发展张力(108g±01g)仍低于对照组(121g±011g,P<005).苯肾上腺素的EC50值(224?
Objective To investigate the relationship between vascular reactivity and nitric oxide (NO) in patients with portal hypertension. Methods Part of the portal vein ligation rats as a model to study the addition and non-nitric oxide synthase inhibitor Nω nitro L arginine (Nω nitro Larginine, L NNA) two cases, The contractile response of isolated abdominal aortic strips to different concentrations of potassium chloride (KCl) (10 mmol / L ~ 80 mmol / L) and phenylephrine (10-9 mol / L ~ 10 -4 mol / L) Results The EC50 values of KCl (265 mmol / L ± 09 mmol / L) were significantly higher than those of the control group (233 mmol / L ± 17 mmol / L, P <001) 37.2nmol / L ± 0.4nmol / L) was also significantly higher than the control group (28.6nmol / L ± 0.2nmol / L, P <0.01). Shrinkage of KCl and phenylephrine in the abdominal aorta of rats with portal vein ligation was decreased. After application of LNNA, the EC50 values of KCl in portal hypertension group and control group were 2118mmol / L ± 08mmol / L and 194mmol / L ± 12mmol / L, respectively, with no significant difference (P > 005). The maximum developmental tension of KCl (108g ± 01g) was still lower than that of the control group (121g ± 011g, P <005). Phenylephrine EC50 value (22 4?