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Previous Volume 339:533-541 August 20, 1998 Number 8 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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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 . . . [Full Text of this Article]

Hemodynamic and Renal Abnormalities in Cirrhosis

Preascitic Cirrhosis

Cirrhosis with Ascites

Nitric Oxide in Animal Models of Cirrhosis

Systemic and Splanchnic Hemodynamic Abnormalities

            Reduced Vasopressor Response to Vasoconstrictors

            Measurement of Nitric Oxide Synthase Activity

            Effects of Inhibition of Nitric Oxide Synthesis

            Expression of Nitric Oxide Synthase in Vascular Tissue

Renal Abnormalities

            Hemodynamic Effects

            Sodium and Water Homeostasis

Summary of Experimental Data

Nitric Oxide in Cirrhosis in Humans

Conclusions

Source Information

From the Department of Medicine, University of Colorado Health Sciences Center, Denver (P.-Y.M., R.W.S.); and the Liver Unit, Hospital Clínic i Provincial, Institut d'Investigacions Biomediques August Pi-Sunyer, Barcelona, Spain (P.G.).

Address reprint requests to Dr. Schrier at the University of Colorado Health Sciences Center, 4200 E. 9th Ave., Denver, CO 80262.

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