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

Ventricular dysfunction in norepinephrine-induced cardiomyopathy

F M Powers1, R Pifarre, J X Thomas

  • 1Department of Physiology, Loyola University Medical Center, Maywood, IL 60153.

Circulatory Shock
|July 1, 1994
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

[Cutaneous tuberculosis caused by Mycobacterium tuberculosis, an uncommon pathology].

Anales de medicina interna (Madrid, Spain : 1984)·2007
Same author

[Pulmonary nocardiosis as a cause of radiographic imaging of multiple pulmonary nodules].

Archivos de bronconeumologia·2001
Same author

[Frequency and risk of bronchopulmonary neoplasia related to asbestos].

Medicina clinica·2001
Same author

The hemostatic effects of warfarin titration in post CABG patients in comparison to placebo treatment.

Journal of thrombosis and thrombolysis·2001
Same author

Northwestern University Medical School.

Academic medicine : journal of the Association of American Medical Colleges·2000
Same author

Inadequacy of current prevention strategies for heparin-induced thrombocytopenia.

Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis·2000
Same journal

Study of septic shock in the non-human primate: relationship of pathophysiological response to therapy with anti-TNF antibody.

Circulatory shock·1994
Same journal

Pentoxifylline inhibits mediator synthesis in an equine in vitro whole blood model of endotoxemia.

Circulatory shock·1994
Same journal

Endocrine and carbohydrate responses to interleukin-6 in vivo.

Circulatory shock·1994
Same journal

Endothelin-1 causes accumulation of leukocytes in the pulmonary circulation.

Circulatory shock·1994
Same journal

Functional requirement of the two TNF receptors for induction of apoptosis in PC60 cells and the role of mitochondria in TNF-induced cytotoxicity.

Circulatory shock·1994
Same journal

Beneficial effects of the phosphodiesterase inhibitors BRL 61063, pentoxifylline, and rolipram in a murine model of endotoxin shock.

Circulatory shock·1994
See all related articles

Norepinephrine infusion acutely impairs rabbit heart function, with systolic function improving within 48 hours, but diastolic function remains impaired. Contractility response to norepinephrine is preserved in these cardiac injury models.

Area of Science:

  • Cardiology
  • Pharmacology
  • Physiology

Background:

  • Norepinephrine-induced cardiomyopathy's effects on cardiac function are not fully understood.
  • Investigating acute and chronic cardiac dysfunction following varying levels of norepinephrine exposure is crucial.

Purpose of the Study:

  • To evaluate acute and chronic changes in systolic and diastolic cardiac function after norepinephrine (NE) infusion.
  • To assess the dose-dependent effects of NE on left ventricular pressure and contractility.
  • To determine the recovery patterns of cardiac function post-NE administration.

Main Methods:

  • Rabbits received intravenous infusions of saline or 2, 4, or 6 µg/kg/min norepinephrine for 90 minutes.
  • Isolated non-ejecting rabbit hearts were used to assess ventricular function immediately post-infusion and at 48 hours.

Related Experiment Videos

  • Hearts were perfused and subjected to varying concentrations of norepinephrine (10⁻¹⁰ to 10⁻⁷ M) to measure left ventricular pressure (LVP), +dP/dt, and -dP/dt.

    • Main Results:

    • Norepinephrine infusion acutely depressed baseline left ventricular systolic function (LVP and +dP/dt) in a dose-dependent manner.
    • By 48 hours, systolic function showed partial recovery, significant only in the 4 µg/kg/min NE group; the 6 µg/kg/min group remained depressed.
    • Diastolic function (-dP/dt) was impaired post-NE infusion and did not recover within 48 hours.
    • Myopathic hearts maintained the ability to increase contractility in response to exogenous norepinephrine.

    Conclusions:

    • Norepinephrine infusion causes acute impairment of both systolic and diastolic left ventricular function.
    • Systolic function shows some recovery within 48 hours, preceding the improvement in diastolic function.
    • The intrinsic ability of the myocardium to increase contractility in response to norepinephrine is not compromised by this injury model.