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

Sustained elevation of norepinephrine depresses hepatocellular function.

P Wang1, S M Tait, I H Chaudry

  • 1Department of Surgery, University of Alabama at Birmingham School of Medicine, 1670 University Boulevard, Volker Hall, Room G094P, Birmingham, AL 35294-0019, USA. ping.wang@ccc.uab.edu

Biochimica Et Biophysica Acta
|December 13, 2000
PubMed
Summary
This summary is machine-generated.

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

Cellular mechanisms of injury after major trauma.

The British journal of surgery·2009
Same author

Castration prevents suppression of MHC class II (Ia) expression on macrophages after trauma-hemorrhage.

Journal of applied physiology (Bethesda, Md. : 1985)·2006
Same author

L-arginine improves wound healing after trauma-hemorrhage by increasing collagen synthesis.

The Journal of trauma·2005
Same author

Differences in the expression of LPS-receptors are not responsible for the sex-specific immune response after trauma and hemorrhagic shock.

Cellular immunology·2004
Same author

Soluble Fas gene therapy protects against Fas-mediated apoptosis of hepatocytes but not the lethal effects of Fas-induced TNF-alpha production by Kupffer cells.

Cell death and differentiation·2002
Same author

Cyclooxygenase-2-mediated regulation of Kupffer cell interleukin-6 production following trauma-hemorrhage and subsequent sepsis.

Shock (Augusta, Ga.)·2002
Same journal

Cumulative Contents.

Biochimica et biophysica acta·2020
Same journal

Molecular Basis of Disease Cumulative Contents.

Biochimica et biophysica acta·2020
Same journal

General Subjects Cumulative Contents.

Biochimica et biophysica acta·2020
Same journal

Erratum to 'on the role of exchangeable hydrogen bonds for the kinetics of P680<sup>+·</sup> Q<sub>A</sub> <sup>-·</sup> formation and P680<sup>+·</sup> Pheo<sup>-·</sup> recombination in photosystem II' [Biochim. Biophys. Acta 1276 (1996) 35-44].

Biochimica et biophysica acta·2019
Same journal

Oligomeric state of the light-harvesting complexes B800-850 and B875 from purple bacterium Rubrivivax gelatinosus in detergent solution.

Biochimica et biophysica acta·2019
Same journal

Regulation of pigment content and enzyme activity in the cyanobacterium Nostoc sp. Mac grown in continuous light, a light-dark photoperiod, or darkness.

Biochimica et biophysica acta·2019
See all related articles

Sustained high levels of norepinephrine (NE) significantly impair liver function and cause injury, even without sepsis or shock. This study demonstrates NE

Area of Science:

  • Physiology
  • Hepatology
  • Pharmacology

Background:

  • Sepsis and hemorrhagic shock activate the sympathetic-adrenal system, increasing catecholamines.
  • Hepatocellular dysfunction during shock correlates with elevated plasma norepinephrine (NE).
  • The direct role of NE in causing hepatocellular dysfunction remains unclear.

Purpose of the Study:

  • To investigate if elevated norepinephrine (NE) alone causes hepatocellular dysfunction.
  • To determine the effects of sustained NE increase on cardiac output, organ perfusion, and liver function.

Main Methods:

  • Exogenous NE was administered via osmotic pumps to mimic shock-related NE levels.
  • Cardiac output, hepatocellular function (indocyanine green clearance Vmax and Km), and organ perfusion were assessed.

Related Experiment Videos

  • Interleukin-6 and liver enzymes were measured.

    • Main Results:

    • Sustained NE elevation decreased cardiac output and microvascular blood flow in the liver, spleen, and intestines.
    • Hepatocellular function (Vmax and Km) was significantly depressed by elevated NE.
    • Increased NE led to elevated liver enzymes and interleukin-6, indicating liver injury.

    Conclusions:

    • Sustained high plasma norepinephrine levels can directly cause hepatocellular dysfunction.
    • Elevated NE contributes to liver injury and altered hepatocyte integrity.
    • These findings highlight NE's critical role in shock-induced liver damage.