Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies
  1. Home
  3. Research Domains
  1. Home
  3. Research Domains

Related Concept Videos

  • Biomedical And Clinical Sciences
  • Oncology And Carcinogenesis
  • Predictive And Prognostic Markers
  • Contribution Of Nitric Oxide To The Pathogenesis Of Cirrhotic Cardiomyopathy In Bile Duct-ligated Rats.
  • Biomedical And Clinical Sciences
  • Oncology And Carcinogenesis
  • Predictive And Prognostic Markers
  • Contribution Of Nitric Oxide To The Pathogenesis Of Cirrhotic Cardiomyopathy In Bile Duct-ligated Rats.

    • Related Experiment Videos

    Contribution of nitric oxide to the pathogenesis of cirrhotic cardiomyopathy in bile duct-ligated rats.

    H Liu1, Z Ma, S S Lee

    • 1Liver Unit, Gastroenterology Research Group, University of Calgary, Calgary, Alberta, Canada.

    Gastroenterology
    |April 28, 2000

    View abstract on PubMed

    Summary
    This summary is machine-generated.

    Nitric oxide (NO) contributes to cirrhotic cardiomyopathy by increasing inducible nitric oxide synthase (NOS2). Inhibiting NOS2 improves cardiac function in cirrhotic rats, suggesting a key role for NO in this condition.

    Related Experiment Videos

    Area of Science:

    • Cardiovascular Physiology
    • Hepatology
    • Molecular Biology

    Background:

    • Cirrhosis is associated with impaired cardiac contractility and beta-adrenergic responsiveness.
    • The underlying mechanisms of cirrhotic cardiomyopathy are not fully understood.
    • Nitric oxide (NO), a known negative inotropic agent, is investigated as a potential contributor.

    Purpose of the Study:

    • To investigate the role of nitric oxide (NO) in the pathogenesis of cirrhotic cardiomyopathy.
    • To examine the expression and activity of nitric oxide synthase (NOS) isoforms in a rat model of cirrhosis.
    • To assess the impact of NO inhibition on cardiac function in cirrhotic rats.

    Main Methods:

    • Cirrhosis was induced in rats via bile duct ligation.
    • Cardiac levels of inflammatory markers (TNF-alpha, IL-1beta), cGMP, and NOS isoforms (NOS2, NOS3) mRNA and protein were quantified.
    • Cardiac function was assessed in isolated papillary muscles, with and without NOS inhibition (L-NAME).

    Main Results:

    • Cirrhotic rats exhibited elevated cardiac TNF-alpha, NOS2, cGMP, and serum IL-1beta and nitrite/nitrate levels compared to controls.
    • Baseline and isoproterenol-stimulated contractility were reduced in cirrhotic rat papillary muscles.
    • NOS inhibition (L-NAME) significantly improved contractility in cirrhotic muscles, while IL-1beta and exogenous NO donors impaired contractility.

    Conclusions:

    • Cytokine-induced stimulation of inducible nitric oxide synthase (NOS2) is implicated in the development of cirrhotic cardiomyopathy.
    • Elevated nitric oxide production contributes to cardiac dysfunction in cirrhosis.
    • Targeting NOS2 may offer a therapeutic strategy for cirrhotic cardiomyopathy.