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

Related Experiment Videos

[Ethanol-induced hepatic microcirculatory disturbance].

Y Takei1, N Sato, T Kamada

  • 1Department of Gastroenterology, Juntendo University School of Medicine, Tokyo, Japan.

Nihon Arukoru Yakubutsu Igakkai Zasshi = Japanese Journal of Alcohol Studies & Drug Dependence
|June 4, 1999
PubMed
Summary

Ethanol causes liver injury by inducing hypoxia through vasoconstriction, primarily in the pericentral liver region. Vasodilators like sodium nitroprusside reduce injury, while endothelin-1 and nitric oxide regulate blood flow.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Chemical change involved in the oxidative-reductive depolymerization of heparin.

Carbohydrate research·1992
Same author

[Relationship between viral hepatitis and alcoholic liver disease].

Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine·1992
Same author

Insulin administration induces capillary growth in brown adipose tissue of heat-exposed rats.

Comparative biochemistry and physiology. Comparative physiology·1992
Same author

Permanent pacemaker implantation in premature infants less than 2,000 grams of body weight.

The Annals of thoracic surgery·1992
Same author

Isolation and characterization of granuloma initiation factor.

The American journal of pathology·1992
Same author

Two cases of variant form angina pectoris associated with myocardial bridge--a possible relationship among coronary vasospasm, atherosclerosis and myocardial bridge.

Japanese circulation journal·1992

Area of Science:

  • Hepatology
  • Vascular Biology
  • Toxicology

Background:

  • Alcoholic liver injury is concentrated in the pericentral liver region, where oxygen levels are naturally lowest.
  • Ethanol metabolism by hepatocytes increases oxygen demand, potentially causing hypoxia.
  • Ethanol can also induce liver hypoxia by disrupting microcirculation.

Purpose of the Study:

  • To investigate the mechanisms by which ethanol induces hepatic hypoxia and injury.
  • To explore the roles of endothelin-1 and nitric oxide in ethanol-induced hepatic vasoconstriction and microcirculatory disturbances.

Main Methods:

  • Isolated perfused rat liver model.
  • Infusion of ethanol at varying concentrations (25-100 mM).
  • Administration of sodium nitroprusside (vasodilator), endothelin-1 antiserum, and NG-monomethyl-L-arginine (nitric oxide synthesis inhibitor).

Related Experiment Videos

  • Monitoring of portal pressure, oxygen consumption, and liver injury.

    • Main Results:

    • Ethanol infusion increased portal pressure in a concentration-dependent manner, indicating vasoconstriction.
    • Sodium nitroprusside reduced ethanol-induced portal pressure increase, enhanced oxygen consumption, and diminished liver injury.
    • Endothelin-1 antiserum inhibited ethanol-induced hepatic vasoconstriction.
    • NG-monomethyl-L-arginine inhibited the 'escape phase' of portal pressure reduction, sustaining vasoconstriction.

    Conclusions:

    • Ethanol-induced hepatic vasoconstriction disrupts liver microcirculation, leading to hypoxia and hepatocellular injury.
    • Endothelin-1 contributes to ethanol-induced vasoconstriction.
    • Nitric oxide plays a role in the resolution of ethanol-induced vasoconstriction.
    • Sinusoidal tone in the presence of ethanol is regulated by endothelin-1 and nitric oxide.