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

Factors involved in left ventricular dysfunction after massive sympathetic activation.

C F Pilati1, F J Bosso, M B Maron

  • 1Department of Physiology, Northeastern Ohio Universities College of Medicine, Rootstown 44272.

The American Journal of Physiology
|September 1, 1992
PubMed
Summary

Massive sympathetic nervous system activation depresses left ventricular function due to toxic catecholamines. Preventing hypertension preserves cardiac function, indicating increased myocardial energy demand contributes to this disorder.

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

beta(2)-adrenergic receptor overexpression increases alveolar fluid clearance and responsiveness to endogenous catecholamines in rats.

Circulation research·2001
Same author

Effect of high transcapillary pressures on capillary ultrastructure and permeability coefficients in dog lung.

Journal of applied physiology (Bethesda, Md. : 1985)·2001
Same author

Importance of behavior in response to tinnitus symptoms.

The international tinnitus journal·2001
Same author

Inactivation of one copy of the mouse neurotrophin-3 gene induces cardiac sympathetic deficits.

Physiological genomics·2000
Same author

Otorhinolaryngological assessment and psychological adjustment in tanning industry workers.

Occupational medicine (Oxford, England)·2000
Same author

Role of angiotensin II in sympathetic nervous system induced left ventricular dysfunction.

Canadian journal of physiology and pharmacology·1999

Area of Science:

  • Cardiovascular Physiology
  • Neuroendocrinology

Background:

  • Massive sympathetic nervous system (SNS) activation can lead to depressed left ventricular (LV) function.
  • The roles of catecholamines and increased myocardial energy demand in this dysfunction are not fully understood.

Purpose of the Study:

  • To determine if catecholamines cause LV dysfunction after SNS activation.
  • To investigate if increased myocardial energy demand from SNS-induced hypertension contributes to LV dysfunction.

Main Methods:

  • Intracisternal veratrine injection in rabbits to activate SNS.
  • In vitro evaluation of LV function 150 minutes post-activation.
  • Assessment of catecholamine involvement using phentolamine and propranolol.
  • Comparison with angiotensin II infusion to mimic SNS hemodynamic profiles.

Related Experiment Videos

Main Results:

  • Massive SNS activation and angiotensin II administration significantly diminished LV function compared to controls (P < 0.01).
  • Pretreatment with catecholamine antagonists prevented LV dysfunction.
  • Maintaining baseline arterial pressure during SNS activation prevented LV dysfunction, suggesting hypertension's role.

Conclusions:

  • Toxic concentrations of catecholamines are responsible for SNS-induced LV dysfunction.
  • Hypertension, likely via increased myocardial energy demand, contributes significantly to depressed cardiac function following SNS activation.