ABSTRACT
Carbon monoxide [CO], an end product of the heme-oxygnase [HO] pathway,is a potent vasodilator and an important modulator of vascular cell function. The present work was designed to study the HO-1/CO system in patients with cirrhosis in relation to severity of liver disease, blood viscosity and splanchnic haemodynamics. Plasma HO-1 levels and blood carboxyhaemoglobin [COHB] concentration,an index of CO production were measured in 30 patients with liver cirrhosis and variable degrees of hepatic dysfunction and in 15 healthy subjects as a controls group. Both patients and control were non smokers. Blood viscosity was measured using the red blood cell pipette viscometer. The blood volume of the portal vein,superior mesenteric artery and splenic artery as well as pusatility index of the arteries were measured using doppler ultrasonography. Plasma [HO-1] levels and blood carboxy haemoglobin concentration were significantly higher in patients with liver cirrhosis than in healthy subjects [p< 0.001]. Also, patients who had esophageal varices, history of bleeding varices, portal hypertensive gastropathy and ascites showed significant increase in HO-1/COHB levels compared with those who did not have these complications [p < 0.001]. The increases in plasma HO-1 level and COHB level showed positive correlation with Child-Pugh score, blood viscosity and the increases in the blood flow volume of the portal vein, superior mesenteric artery and splenic artery and inverse correlation with the decreases in the pulsatility index and the resistive index of the arteries in patients with liver cirrhosis [P< 0.05]. Increased HO-1 activity with enhanced endogenous CO generation may play a role in the development of splanchnic vasodilation and serious manifestations of portal hypertension in liver cirrhosis