Pulmonary-Hepatic vascular Disorders (PHD)

Rodríguez-Roisín, Robert; Krowka, Michael J.; Hervé, P; Fallon, Michael B.

doi:10.1183/09031936.04.00010904

Cited by 699 publications

(660 citation statements)

References 284 publications

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“…An elevation of the serum level of IL-8 has also been observed in patients with nonalcoholic steatohepatitis (30) and those with alcoholic liver disease (31) (1,32). It has been reported that the exhaled NO level is increased in liver cirrhosis (33,34), and the expression of pulmonary vascular NO synthase (NOS) is increased in hepatopulmonary syndrome (35)(36)(37) …”

Section: Smoking Is a Major Risk Factor For Copd And Aging Increases mentioning

confidence: 89%

Prevalence of COPD in Primary Care Clinics: Correlation with Non-Respiratory Diseases

et al. 2008

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Background and Objective Various extrapulmonary effects and comorbidities have been noted to contribute to the burden of chronic obstructive pulmonary disease (COPD). However, the relationship between the prevalence of COPD and non-respiratory diseases has not been well investigated. The aim of the present study was to determine whether or not COPD is different among patients already suffering from other diseases.

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Section: Smoking Is a Major Risk Factor For Copd And Aging Increases mentioning

confidence: 89%

Prevalence of COPD in Primary Care Clinics: Correlation with Non-Respiratory Diseases

et al. 2008

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“…However, the presence of spider nevi, digital clubbing, cyanosis and severe hypoxemia (PaO2 b60 mmHg) strongly suggests a diagnosis of this condition. Orthodeoxia and platypnea seem to be further associated with ventilation-perfusion mismatch [61,59]. A chest radiograph is not adequate.…”

Section: Pulmonary Complications 261 Hepatopulmonary Syndromementioning

confidence: 99%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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The hyperdynamic syndrome is a late consequence of portal hypertension in cirrhosis. The principal hemodynamic manifestations of the hyperdynamic syndrome are high cardiac output, and increased heart rate and total blood volume, accompanied by reduced total systemic vascular resistance. Pathophysiology involves a complex of humoral and neural mechanisms that can determine hemodynamic changes, and lead to hyperdynamic circulation. In this review we focus our attention on the manifestations of the hyperdynamic syndrome. Some of these are well described and directly related to portal hypertension (varices, ascites, hepatic encephalopathy, and hepatorenal syndrome), while others, such as hepatopulmonary syndrome, portopulmonary hypertension, and cirrhotic cardiomyopathy, are less known as clinical manifestations related to cirrhosis and, therefore, merit further investigation.

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“…1 Arterial deoxygenation in HPS is caused by ventilation-perfusion mismatching and intrapulmonary shunt along with a diffusion-perfusion defect in most advanced cases. 2 Few experimental and clinical evidences in HPS suggest that enhanced pulmonary production of nitric oxide (NO) plays a key role in the development of intrapulmonary vascular dilatations.…”

Section: See Editorial On Page 912mentioning

confidence: 99%

“…HPS was defined when, along with a diagnosis of liver disease, patients showed (1) increased alveolar-arterial oxygen gradient of 15 mm Hg or more while breathing room air in an upright position, with or without arterial hypoxemia (arterial oxygen tension Ͻ80 mm Hg), and (2) evidence of intrapulmonary vascular dilatations using transthoracic contrast-enhanced echocardiography. 1 The study was approved by the ethical committee of our institution, and all patients gave written informed consent to participate.…”

Section: Populationmentioning

confidence: 99%

Effects of nebulizedNG-nitro-L-arginine methyl ester in patients with hepatopulmonary syndrome

et al. 2006

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Enhanced pulmonary production of nitric oxide (NO) has been implicated in the pathogenesis of hepatopulmonary syndrome (HPS). NO inhibition with N G -nitro-L-arginine methyl ester (L-NAME) in both animals and humans with HPS has improved arterial hypoxemia. We assessed the role of enhanced NO production in the pathobiology of arterial deoxygenation in HPS and the potential therapeutic efficacy of selective pulmonary NO inhibition. We investigated the effects of nebulized L-NAME (162.0 mg) at 30 and 120 minutes on all intrapulmonary and extrapulmonary factors governing pulmonary gas exchange in 10 patients with HPS (60 ؎ 7 [SD] yr; alveolar-arterial oxygen gradient, range 19-76 mm Hg; arterial oxygen tension, range 37-89 mm Hg). Nebulized L-NAME maximally decreased exhaled NO (by ؊55%; P < .001), mixed venous nitrite/nitrate (by ؊12%; P ‫؍‬ .02), and cardiac output (by ؊11%; P ‫؍‬ .002) while increased systemic vascular resistance (by 11%; P ‫؍‬ .008) and pulmonary vascular resistance (by 25%; P ‫؍‬ .03). In contrast, ventilation-perfusion mismatching, intrapulmonary shunt and, in turn, arterial deoxygenation remained unchanged. In conclusion, gas exchange disturbances in HPS may be related to pulmonary vascular remodeling rather than to an ongoing vasodilator effect of enhanced NO production. ( H epatopulmonary syndrome (HPS) is defined as an arterial oxygenation defect induced by intrapulmonary vascular dilatations associated with hepatic disease. 1 Arterial deoxygenation in HPS is caused by ventilation-perfusion mismatching and intrapulmonary shunt along with a diffusion-perfusion defect in most advanced cases. 2 Few experimental and clinical evidences in HPS suggest that enhanced pulmonary production of nitric oxide (NO) plays a key role in the development of intrapulmonary vascular dilatations. [3][4][5][6][7][8][9][10] Morphologically, the striking feature in HPS is widespread dilatation and increased number of pulmonary capillaries in alveolar regions 11 that suggest a vasculogenic rather than a vasoactive pathobiological process. 12 Studies with NO inhibitors in HPS, however, have highlighted that active NO-dependent pulmonary vasodilatation may contribute to the persistence of gas exchange abnormalities. 10,13,14 In patients with HPS, there was a transient improvement in arterial oxygenation after intravenous methylene blue, an inhibitor of soluble guanylate cyclase and cyclic guanosine monophosphate production, a final molecular step for NO-mediated vasorelaxation. 13,14 Similarly, inhibition of NO synthase with nebulized N G -nitro-L-arginine methyl ester (L-NAME) in a patient with HPS improved arterial oxygen tension, 15 suggesting that the selective inhibition of pulmonary NO through the inhaled route could be of potential therapeutic benefit. Nevertheless, the precise role of a NO-dependent pulmonary vasodilatation involved in the pathogenesis of abnormal pulmonary gas exchange in HPS remains far from clear.To shed further light into the pathogenesis of HPS and to explore the potential therapeutic a...

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Pulmonary-Hepatic vascular Disorders (PHD)

Cited by 699 publications

References 284 publications

Prevalence of COPD in Primary Care Clinics: Correlation with Non-Respiratory Diseases

Prevalence of COPD in Primary Care Clinics: Correlation with Non-Respiratory Diseases

Clinical implications of the hyperdynamic syndrome in cirrhosis

Effects of nebulizedNG-nitro-L-arginine methyl ester in patients with hepatopulmonary syndrome

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