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  • Title: Vasopressin response and shunting modulation in cirrhotic rats by chronic nitric oxide inhibition.
    Author: Huang HC, Wang SS, Lee FY, Chang CC, Chang FY, Lin HC, Hou MC, Lee SD.
    Journal: J Gastroenterol Hepatol; 2008 Jul; 23(7 Pt 2):e265-9. PubMed ID: 17764528.
    Abstract:
    BACKGROUND AND AIM: Nitric oxide (NO) plays a significant role in the vascular hyposensitivity to vasoconstrictors in cirrhosis. Chronic NO inhibition improves the portal-systemic collateral responsiveness to arginine(8)-vasopressin (AVP) and ameliorates shunting degree in rats with prehepatic portal hypertension. This study investigated whether long-term NO inhibition by N(G)-nitro-L-arginine methyl ester (L-NAME) enhances the collateral vascular responsiveness to AVP and alleviates the severity of shunting in cirrhotic rats. METHODS: Bile duct-ligated (BDL) rats received L-NAME in tap water (25 mg/kg/day) or tap water only (control) for 1 week from the 36th day after BDL. On the 43rd day, the mean arterial pressure and portal pressure were measured. With an in situ perfusion model of portal-systemic collateral vasculature, different concentrations of AVP (10(-10)-10(-7) mol/L) with a constant flow rate (12 mL/min) were applied to assess the perfusion pressure changes of collaterals. In addition, flow pressure curves were obtained with different flow rates (6-18 mL/min): the slopes serve as indices of collateral vascular resistance and the higher resistance indicates less collateral. RESULTS: The mean arterial pressure was significantly increased after L-NAME treatment (P < 0.05), whereas the heart rate and portal pressure were not significantly modified. As compared with the controls, the L-NAME group exerted significantly higher perfusion pressure changes to AVP at the concentrations of 3 x 10(-8), 10(-7) and 3 x 10(-7) mol/L. In addition, chronic L-NAME administration induced collateral vascular resistance elevation, suggesting the attenuation of portal-systemic shunting. CONCLUSION: Chronic NO inhibition improves the collateral vascular responsiveness to AVP and ameliorates portal-systemic shunting in BDL cirrhotic rats.
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