ENDOGENOUS NITRIC-OXIDE PRODUCTION IS AUGMENTED AS THE SEVERITY ADVANCES IN PATIENTS WITH LIVER-CIRRHOSIS

1. Since endothelium-derived nitric oxide (NO) is a potent vasodilator and degraded into nitrous ions, we measured the serum nitrate ion (NO 3-) and the amount of urinary excretions of NO3- as an index for endog enous NO to ascertain whether NO formation is augmented in patients wi th chronic liver diseases. 2. Using inpatients suffering from chronic liver diseases, serum levels and urinary excretions of NO3- were measu red by using high-performance liquid chromatography with an anion exch ange column, 3. Among the four patient groups of normal controls, and those with chronic liver diseases such as chronic active hepatitis, co mpensated cirrhosis, and decompensated cirrhosis the serum level of NO 3- showed the highest level in a patient group with decompensated cirr hosis. The amount of urinary excretion of NO3- was significantly incre ased in both groups of patients with liver cirrhosis compared with the control group and patients with chronic active hepatitis. Patients wi th chronic active hepatitis did not show any difference between the no rmal control group. The amount of urinary excretion of NO3- correlated significantly and negatively with the level of serum albumin (P < 0.0 5) and counts of platelets (P < 0.01) in patients with compensated cir rhosis. 4. These findings suggest that the production of endogenous NO is augmented in patients with liver cirrhosis, particularly in a deco mpensated subgroup. Increases in the production of endogenous NO corre spond to the progress of liver cirrhosis, but not in patients with chr onic hepatitis.