when cirrhosis is decompensated. [2][3][4][5][6] In vivo studies using veNitric oxide production was studied in cirrhotic panous occlusion plethysmography have shown an overproductients with spontaneous bacterial peritonitis (SBP) or tion of NO related to the hyporesponsiveness to vasoconstricwith other infections. We followed up on the time course tors in cirrhotic patients. 7 However, which specific isoform of of serum nitrate levels in 51 hospitalized patients aged NOS accounts for this increment has not been clearly deterbetween 34 and 81 years. Four groups were defined: pamined. To explain vasodilation in cirrhotic patients, Vallance tients with SBP (group 1, n Å 14), patients with bacterand Moncada have hypothesized that endotoxemia might inemia (group 2, n Å 11), patients with urinary tract infecduce the synthesis and release of NO by iNOS, either directly tion (group 3, n Å 11) and patients in a stable clinical or indirectly via cytokines, and this might therefore account condition (group 4, n Å 20). The four groups did not differ for the hyperdynamic circulatory syndrome associated with in terms of Pugh score (11 { 1, 10 { 1, 11 { 1, and 10 { cirrhosis. 8 This is supported by the findings of Guarner et al. 1, respectively). Serum nitrate levels averaged 31 { 2 that serum levels of nitrate correlated with those found in mmol/L in group 4 (84 samples). On the day results of endotoxemia. 4 On the other hand, endothelial constitutive cytobacteriological examination were positive, mean se-NOS was reported to be up-regulated in rats with CCl 4 -inrum nitrate levels were 75 { 17, 63 { 9, and 36 { 9 mmol/ duced cirrhosis, which suggests a major role of this isoform L, respectively, in groups 1 (17 cases), 2 (11 cases), and in the increased production of NO in cirrhotic rats. 9 The last 3 (11 cases) (P õ .001). The maximum nitrate values repossibility is that both isoforms are involved: a mechanical corded during follow-up were higher in groups 1 (149 { stimulation of endothelial constitutive NOS might be second-15 mmol/L) and 2 (112 { 11 mmol/L) than in group 3 (66 ary to increased cardiac output and shear stress, whereas { 7 mmol/L; P õ .001 and õ.01, respectively). These maxianother source of NO might be from iNOS stimulated biomum values were recorded in all groups approximately chemically through cytokines or endotoxins. weeks after the infection was diagnosed. The meanIn a previous study, we found that 1) patients with ascites duration of NO overproduction, as defined by nitrate had higher nitrate levels than those without ascites and 2) level 3 90 mmol/L, was 15 { 3 days in group 1 and 5 { 1 nitrate levels correlated with orosomucoid, a protein of the day in group 2. When the nitrate concentration was studacute-phase response, which suggests that increased nitrate ied in serum and ascitic fluid sampled on the same day, levels were related to activation of iNOS. 6 The high prevait was found to be higher in ascitic fluid than in serum lence of infectious complications in cirrhotic patients with in eight ca...