Campillo B, Bories P N, Benvenuti C, Dupeyron C
Service d'Hépato-gastroentérologie et Rééducation Digestive, Hôpital Albert Chenevier, Créteil, France.
J Hepatol. 1996 Nov;25(5):707-14. doi: 10.1016/s0168-8278(96)80242-x.
BACKGROUND/AIMS: The relationship between nitric oxide production, endotoxemia, renal function and hyperdynamic circulatory syndrome has not been yet investigated in patients with cirrhosis.
Serum and urine nitrate, endotoxemia and cardiac index were measured in 59 patients with cirrhosis.
Patients with a tense ascites had higher serum nitrate levels than healthy control subjects (39 +/- 7 vs 19 +/- 4 mumol/l, p < 0.01). Patients with mild ascites and without ascites had normal values of nitrate levels. In the group of patients not treated with diuretics (n = 38), creatinine and nitrate clearances were lower in ascitic patients than in nonascitic patients (respectively 0.82 +/- 0.12 vs 1.48 +/- 0.32 ml/s, p < 0.02 and 0.30 +/- 0.07 vs 2.89 +/- 2.04 ml/s, p < 0.05). Endotoxin levels were higher in patients with cirrhosis than in control subjects and paralleled the severity of liver failure (Child A/B/C vs control subjects: 0.056 +/- 0.014/0.064 +/- 0.005/ 0.090 +/- 0.008 vs 0.027 +/- 0.005 Endotoxin Units/ml, p < 0.001). Serum nitrate levels did not correlate with endotoxemia (r = -0.110). On the other hand, levels of orosomucoid, a protein synthesized by the liver in response to a stimulation by cytokines correlated with those of nitrate (respectively r = 0.343, p < 0.01). Hemoglobin levels were negatively correlated with serum nitrate levels (r = -0.328 p < 0.02). Cardiac index was higher in patients than in control subjects and paralleled the degree of liver failure (Child A/B/C vs control subjects: 3.60 +/- 0.25/ 4.10 +/- 0.19/4.47 +/- 0.25 vs 3.15 +/- 0.12 l.min.m2, p < 0.001). Cardiac index did not correlate with serum nitrate levels, urine nitrate excretion and endotoxemia.
Renal impairment accounts for the increased levels of serum nitrate in ascitic patients. A stimulation of nitric oxide production by cytokines may occur but endotoxemia is not involved in such a mechanism. Anemia has a role in nitric oxide activity. Nitric oxide generation assessed by nitrate in serum and urine does not seem to participate in the hyperdynamic circulatory syndrome in patients with cirrhosis.
背景/目的：尚未对肝硬化患者一氧化氮生成、内毒素血症、肾功能和高动力循环综合征之间的关系进行研究。
对59例肝硬化患者测定血清和尿液硝酸盐、内毒素血症及心脏指数。
有张力性腹水的患者血清硝酸盐水平高于健康对照者（39±7 vs 19±4 μmol/L，p<0.01）。轻度腹水和无腹水的患者硝酸盐水平正常。在未接受利尿剂治疗的患者组（n = 38）中，腹水患者的肌酐清除率和硝酸盐清除率低于无腹水患者（分别为0.82±0.12 vs 1.48±0.32 ml/s，p<0.02；0.30±0.07 vs 2.89±2.04 ml/s，p<0.05）。肝硬化患者的内毒素水平高于对照者，且与肝功能衰竭的严重程度平行（Child A/B/C vs对照者：0.056±0.014/0.064±0.005/0.090±0.008 vs 0.027±0.005内毒素单位/ml，p<0.001）。血清硝酸盐水平与内毒素血症无相关性（r = -0.110）。另一方面，肝脏在细胞因子刺激下合成的一种蛋白质——血清类黏蛋白的水平与硝酸盐水平相关（r分别为0.343，p<0.01）。血红蛋白水平与血清硝酸盐水平呈负相关（r = -0.328，p<0.02）。患者的心脏指数高于对照者，且与肝功能衰竭程度平行（Child A/B/C vs对照者：3.60±0.25/4.10±0.19/4.47±0.25 vs 3.15±0.12 l·min·m²，p<0.001）。心脏指数与血清硝酸盐水平、尿硝酸盐排泄及内毒素血症均无相关性。
肾功能损害导致腹水患者血清硝酸盐水平升高。细胞因子可能刺激一氧化氮生成，但内毒素血症不参与这一机制。贫血对一氧化氮活性有影响。通过血清和尿液中的硝酸盐评估的一氧化氮生成似乎不参与肝硬化患者的高动力循环综合征。
