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Temporal changes in left ventricular function after massive sympathetic nervous system activation

S A Lang1, M B Maron, F J Bosso

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

Canadian Journal of Physiology and Pharmacology
|June 1, 1994
PubMed
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Massive sympathetic nervous system (SNS) activation significantly reduces left ventricular (LV) contractility in dogs. This cardiac dysfunction occurs rapidly and persists, independent of initial blood pressure changes.

Area of Science:

  • Cardiovascular Physiology
  • Autonomic Nervous System Research

Background:

  • The sympathetic nervous system (SNS) plays a crucial role in regulating cardiac function.
  • Previous studies suggest SNS activation can impair left ventricular (LV) contractility.

Purpose of the Study:

  • To investigate the time course and characteristics of LV dysfunction following massive central SNS activation in dogs.
  • To differentiate the effects of SNS activation from mere hypertensive responses on LV contractility.

Main Methods:

  • Central SNS activation was induced via intracisternal veratrine injection in anesthetized dogs.
  • Hemodynamic parameters including LV end-diastolic pressure (LVEDP), cardiac output, heart rate, and aortic pressure (Pa) were monitored.
  • LV function curves were analyzed to assess contractility changes.

Related Experiment Videos

  • Plasma catecholamine levels were measured.
  • Control groups included time-matched controls and dogs with aortic constriction to mimic hypertension.

    • Main Results:

    • Intracisternal veratrine rapidly increased aortic pressure and markedly decreased LV contractility, evidenced by shifts in LV function curves.
    • The observed LV dysfunction persisted for 3 hours, outlasting the initial hypertensive phase.
    • Plasma catecholamine concentrations significantly increased after SNS activation.
    • Aortic constriction alone resulted in only modest changes in LV function.

    Conclusions:

    • Massive SNS activation leads to a rapid and sustained decline in myocardial contractility.
    • The observed LV dysfunction is a direct consequence of SNS activation, not solely due to the associated hypertension.
    • Elevated catecholamines likely contribute to the observed myocardial depression.