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Cited by 446

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Nitric Oxide as a Mediator of Hemodynamic Abnormalities and Sodium and Water Retention in Cirrhosis

Martin, Pierre-Yves, Ginès, Pere, Schrier, Robert W.·1998·New England Journal of Medicine

Abstract

A decade ago, it was proposed that peripheral arterial vasodilation was an important event in the pathophysiology of ascites formation in patients with cirrhosis.1 At the same time, nitric oxide was demonstrated to be a potent vasodilator with a major role in the regulation of vascular tone,2 and it was hypothesized that nitric oxide could be the cause of the hyperdynamic circulation of patients with cirrhosis.3 Since then, studies in animals and humans with portal hypertension have provided evidence suggesting that nitric oxide has an important role in the hemodynamic abnormalities that characterize cirrhosis and the associated sodium and water . . .

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Metadata

Authors
Martin, P.-Y., Ginès, P., & Schrier, R. W.
Venue
New England Journal of Medicine
Published
1998-08-20
Volume
339
Issue
8
Pages
533-541
ISSN
  • 0028-4793 (ISSN-L)
  • 1533-4406
OpenAlex
W2338255346
Cited by
446
References
0
FWCI
17.16
Type
journal article
Language
en
Open access
closed

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.