Increased Nitric Oxide in the Exhaled Air of Patients with Decompensated Liver Cirrhosis

Matsumoto, Akira; Ogura, Keiji; Hirata, Yasunobu; Kakoki, Masao; Watanabe, Fumiyoshi; Takenaka, Katsu; Shiratori, Yasushi; Momomura, Shin‐ichi; Omata, Masao

doi:10.7326/0003-4819-123-2-199507150-00005

Cited by 112 publications

(63 citation statements)

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“…13 Nevertheless, the level of NO during exhalation differs in various pathophysiologic conditions; for examples, it is increased in patients with asthma, 23,24 bronchiectasis, 25 systemic lupus erythematosus, 26 and liver cirrhosis. 27,28 NO levels were also found to increase with exercise, 29,30 during the mid menstrual cycle in women, 31 and during pregnancy. 32 Conversely, NO was reduced with ethanol ingestion.…”

Section: Discussionmentioning

confidence: 84%

Reduced production of nitric oxide during haemodialysis

Sumino

Sato

Sakamaki³

et al. 1999

J Hum Hypertens

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Objective: To examine the influence of systemic nitric oxide (NO) synthesis on blood pressure in patients with chronic renal failure undergoing haemodialysis, since nitric oxides are susceptible to renal excretion or are dialysed, a different indicator that is unaffected by renal function, such as the level of exhaled NO was evaluated. We examined the levels of the endogenous NO before and after a haemodialysis session. Design and methods: We evaluated the serum concentrations of nitrite/nitrate and the rate of nitric oxide release into exhaled air in 10 patients with hypertension who were receiving maintenance haemodialysis. Results: The serum concentrations of nitrite/nitrate before haemodialysis were significantly higher than those in 10 normal controls (183 ؎ 151 M vs 42 ؎ 17 M, P Ͻ 0.05). These levels decreased signifi-

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Section: Discussionmentioning

confidence: 84%

Reduced production of nitric oxide during haemodialysis

Sumino

Sato

Sakamaki³

et al. 1999

J Hum Hypertens

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“…Exhaled NO concentrations, which reflect NO production in the airways [15], are higher in advanced cirrhosis [16][17][18][19][20] than in patients with compensated cirrhosis or in normal subjects. Moreover, patients with decompensated cirrhosis have higher serum levels of nitrites and nitrates [5,20] than do patients with compensated cirrhosis and normal subjects.…”

Section: Haemodynamics In Cirrhosis With Portal Hypertensionmentioning

confidence: 99%

Pulmonary vascular disorders in portal hypertension

Hervé

Lebrec²,

Brénot³

et al. 1998

Eur Respir J

326

239

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aaThis review focuses on the pulmonary vascular complications of chronic liver failure and portal hypertension. The wide spectrum of pulmonary vascular disorders in liver disease and portal hypertension ranges from the hepatopulmonary syndrome (HPS), which is characterized by intrapulmonary vascular dilatations, to pulmonary hypertension (portopulmonary hypertension), in which pulmonary vascular resistance (PVR) is elevated. The exact pathophysiological mechanisms of these pulmonary vascular disorders are unknown. However, since HPS and portopulmonary hypertension have been reported in patients with nonhepatic portal hypertension, the factor that determines their development must be portal hypertension.A brief review of the haemodynamic changes observed in cirrhosis with portal hypertension is summarized, and the clinical and experimental evidence suggesting that the liver exerts a critical influence on the regulation of pulmonary vascular tone and angiogenesis is described. Portopulmonary hypertension is then discussed, focusing in turn on its clinical presentations, management and potential mechanisms, and referring to our findings in 39 patients with portopulmonary hypertension and 140 patients with primary pulmonary hypertension (PPH) admitted between 1986 and 1996 at Antoine Béclère Hospital. Finally, HPS will be examined, with a discussion of the mechanisms of hypoxaemia and intrapulmonary vascular dilatation, as well as its clinical presentation, diagnosis and treatment, with special attention to liver transplantation. Haemodynamics in cirrhosis with portal hypertensionAn understanding of pulmonary haemodynamics in liver disease with portal hypertension is important to a study of the pulmonary vascular disorders seen in this setting. A hyperdynamic circulatory state with high cardiac output, low systemic vascular resistance and low PVR is present in 30-50% of patients with cirrhosis and also in animal models of portal hypertension [1][2][3][4]. Compared with healthy subjects ( fig. 1) The wide spectrum of pulmonary vascular disorders in liver disease and portal hypertension ranges from the hepatopulmonary syndrome characterized by intrapulmonary vascular dilatations, to pulmonary hypertension (portopulmonary hypertension), in which pulmonary vascular resistance is elevated. Since hepatopulmonary syndrome and portopulmonary hypertension have been reported in patients with nonhepatic portal hypertension, the common factor that determines their development must be portal hypertension. The clinical presentations are very different, with gas exchange impairment in the hepatopulmonary syndrome and haemodynamic failure in portopulmonary hypertension. The severity of hepatopulmonary syndrome seems to parallel the severity of liver failure, whereas no simple relationship has been identified between hepatic impairment and the severity of portopulmonary hypertension. Resolution of hepatopulmonary syndrome is common after liver transplantation, which has an uncertain effect in portopulmonary hypertension. The pathoph...

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“…Serum nitrite/nitrate levels are increased in liver cirrhosis and this is related to endotoxaemia [100]. Increased exhaled NO levels, derived from the alveolar region [101,102], are observed in patients with advanced cirrhosis with and without HPS [57,58,103], and correlate with the abnormally increased PA-a,O 2 [57] and high Q9 [103]. Partial or complete resolution of clinical and functional markers of HPS after using different inhibitors and/or interventions that block the effects of NO, such as methylene blue [59,104] and L-NAME [105], or following smoking [106] and OLT [56], sporadically or anecdotally reported, support the idea that increased endogenous pulmonary NO could play a pivotal role in the development of arterial deoxygenation.…”

Section: Clinical Diagnosismentioning

confidence: 99%