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ENDOGENOUS NITRIC OXIDE PRODUCTION IS AUGMENTED AS THE SEVERITY ADVANCES IN PATIENTS WITH LIVER CIRRHOSIS
Author(s) -
Hori Naoki,
Okanoue Takeshi,
Mori Takashi,
Kashima Kei,
Nishimura Masato,
Nanbu Akira,
Yoshimura Manabu,
Takahashi Hakuo
Publication year - 1996
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1996.tb03058.x
Subject(s) - cirrhosis , medicine , gastroenterology , endogeny , excretion , nitric oxide , urinary system , albumin , hepatitis , endocrinology
SUMMARY1 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 NO 3 − as an index for endogenous NO to ascertain whether NO formation is augmented in patients with chronic liver diseases. 2 Using inpatients suffering from chronic liver diseases, serum levels and urinary excretions of NO 3 − were measured by using high‐performance liquid chromatography with an anion exchange column. 3 Among the four patient groups of normal controls, and those with chronic liver diseases such as chronic active hepatitis, compensated cirrhosis, and decompensated cirrhosis the serum level of NO 3 − showed the highest level in a patient group with decompensated cirrhosis. The amount of urinary excretion of NO 3 − was significantly increased in both groups of patients with liver cirrhosis compared with the control group and patients with chronic active hepatitis. Patients with chronic active hepatitis did not show any difference between the normal control group. The amount of urinary excretion of NO 3 − correlated significantly and negatively with the level of serum albumin ( P <0.05) and counts of platelets ( P < 0.01) in patients with compensated cirrhosis. 4 These findings suggest that the production of endogenous NO is augmented in patients with liver cirrhosis, particularly in a decompensated subgroup. Increases in the production of endogenous NO correspond to the progress of liver cirrhosis, but not in patients with chronic hepatitis.