Exhaled nitric oxide and oxygenation abnormalities in hepatic cirrhosis

Impaired arterial oxygenation, ranging from increased alveolar-arterial oxygen gradient (AaDo(2)) to hypoxemia, is commonly present in patients with cirrhosis. Nitric oxide (NO), through pulmonary vasodilatation, may play a major role in the oxygen abnormalities of cirrhosis, Our aim was to study the relationship between NO production and O-2 abnormalities in 45 nonsmoking patients with cirrhosis and without major cardiovascular and respiratory diseases. Intrapulmonary shunting was detected by contrast-enhanced (CE) echocardiography, Lung volumes and diffusion, arterial blood gas analysis, serum NO2-/NO3-, NO output in the exhaled air, and cardiac index by the echocardiographic method were determined in all patients. Twenty-seven (60%) patients had an abnormally increased (>15 mm Hg) AaDo(2). The mean values of exhaled NO output and serum NO2-/NO3- were significantly higher in cirrhotic patients than in controls (252 +/- 117 vs. 75.2 +/- 19 nL/min/m(2), P < .0001; and 47.5 +/- 29.4 vs. 32.9 +/- 10.1 mu mol/L, P < .02, respectively), In all patients, there was a significant correlation between exhaled NO and AaDo(2) (r = .78, P < .0001). Twelve patients (26.6%) were found to have CE-echocardiographic evidence of intrapulmonary shunting (positive CE-echo). Nine patients were considered to have hepatopulmonary syndrome (HPS) on the basis of an AaDo(2) > 15 mn Hg and positive CE-echo. These 9 patients had a mean value of exhaled NO significantly higher than patients without LIPS (331 +/- 73.2 vs. 223 +/- 118.4 nL/min/m(2), P < .05). In all patients, cardiac index was positively correlated with exhaled NO (r = .47, P < .001) and with serum NO2-/NO3- (r = .43, P < .01). The results suggest an important role of NO in the oxygenation and circulatory abnormalities of patients with cirrhosis.