摘要
ＯｖｅｒｐｒｏｄｕｃｔｉｏｎｏｆｎｉｔｒｉｃｏｘｉｄｅｉｎｈｉｂｉｔｓｖａｓｃｕｌａｒｒｅａｃｔｉｖｉｔｙｉｎｐｏｒｔａｌｈｙｐｅｒｔｅｎｓｉｖｅｒａｔｓＬＩＸｉＲｕ，ＷＵＪｉｎＳｈｅｎｇ，ＨＥＺｅＳｈｅｎｇ，ＭＡＱｉｎｇＪｉｕａｎｄＧＡＯ...
IM To evaluate the relationship between nitric oxide (NO) and hyperdynamic circulatory status in portal hypertension.METHODS Twenty male SpragueDawley rats (weighing 200g±20g) randomized into two groups, portal hypertension group (n=12) and the controls (n=8). Portal hypertensive models were established by means of graded constriction of the portal vein. The concentrations of nitrite (NO2) in portal vein and peripheral blood were measured to reflect NO levels with flourimetric analysis. The reactivitiy of isolated abdominal aortic rings from partial portal veinconstricted and shamoperated rats was observed by potassium chloride (KCl) (10mmol/L-80mmol/L) and phenylephrine (10-9mol/L10-4mol/L) with or without NO synthase inhibitor NωnitroLarginine (LNNA).RESULTS Serum concentrations of NO2 in portal vein (0766μmol/L±0097μmol/L) and peripheral blood (0687μmol/L±0092μmol/L) were elevated in portal hypertensive rats as compared with those in controls (0613μmol/L±0084μmol/L, 0591μmol/L±0045μmol/L, P<001, respectively). The rates of NO2 in portal vein blood were markedly higher than those in peripheral blood (P<005) of portal hypertensive rats. Abdominal aortic rings from portal veinconstricted rats exhibited significantly impaired contractility to phenylephrine and potassium chloride as compared with the controls. The EC50 values of KCl were markedly higher in portal hypertensive rings (265mmol/L±09mmol/L) than those of the control rings (223mmol/L±17mmol/L, P<001), and so were the EC50 values of phenylephrine (372nmol/L±04nmol/L) vs (281nmol/L±02nmol/L, P<001). After preincubation of rings with LNNA, the difference in EC50 values no longer statistically significant between portal hypertensive and control rings in both KCl (2018mmol/L±08mmol/L, and 194mmol/L±12mmol/L, P>005) and phenylephrine (224nmol/L±18nmol/L, 218nmol/L±14nmol/L, P>005). However, the maximal KCl and phenylephrineinduced contractions were still lower in portal hypertensive rings (KCl: 108g±01g, phenylephrine: 143g±014g) than those of the control rings (KCl: 121g±011g, phenylephrine: 172g±011g, P<005, respectively). This showed that addition of the NO synthase inhibitor LNNA could partially restore contractile responses to KCl and phenylephrine in portal hypertensive rings.CONCLUSION NO overproduction inhibits the vascular reactivity to vasocontrictors, and it might be one of the main causes which results in vasodilatation and hyperdynamic circulatory status in portal hypertension.
