The hyperdynamic circulation of chronic liver diseases: From the patient to the molecule

Authors

  • Yasuko Iwakiri,

    1. Hepatic Hemodynamic Laboratory, VA Connecticut Healthcare System, West Haven, CT
    2. Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT
    3. Department of Pharmacology, Yale University School of Medicine, New Haven, CT
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  • Roberto J. Groszmann

    Corresponding author
    1. Hepatic Hemodynamic Laboratory, VA Connecticut Healthcare System, West Haven, CT
    2. Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT
    • Digestive Disease Section/111H, VA Medical Center, 950 Campbell Avenue, West Haven, CT 06516
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    • fax: 203-937-3873.


  • Potential conflict of interest: Nothing to report.

Abstract

The hyperdynamic circulatory syndrome observed in chronic liver diseases is a great example of research that originated from clinical observations and progressed in the last 50 years from the patient to the experimental laboratory. Our knowledge has evolved from the patient to the molecule, using experimental models that serve as a source for understanding the complex pathophysiological mechanisms that govern this complex syndrome. We now know that progressive vasodilatation is central to the detrimental effects observed in multiple organs. Although nitric oxide has been shown to be the primary vasodilator molecule in these effects, other molecules also participate in the complex mechanisms of vasodilatation. This review summarizes three major areas: first, clinical observation in patients; second, experimental models used to study the hyperdynamic circulatory syndrome; and third, the vasodilator molecules that play roles in vascular abnormalities observed in portal hypertension. (Hepatology 2006;43:S121–S131.)

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