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Parasympathetic neurons in the cranial medial ventricular fat pad on the dog heart selectively decrease ventricular

L W Dickerson1, D J Rodak, T J Fleming

  • 1Department of Pharmacology, Georgetown University School of Medicine, Washington, DC 20007, USA.

Journal of the Autonomic Nervous System
|August 1, 1998
PubMed
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Parasympathetic ganglia in the cranial medial ventricular (CMV) fat pad selectively control ventricular contractility. Blocking these ganglia reduced negative inotropic effects of vagal stimulation without impacting heart rate or AV conduction.

Area of Science:

  • Cardiovascular Physiology
  • Autonomic Nervous System Research
  • Cardiac Electrophysiology

Background:

  • The autonomic nervous system regulates cardiac function through sympathetic and parasympathetic pathways.
  • The precise neural mechanisms controlling ventricular contractility, particularly parasympathetic influences, remain incompletely understood.
  • Previous research suggests localized neural control centers may exist within cardiac ganglia.

Purpose of the Study:

  • To investigate the role of the cranial medial ventricular (CMV) ganglion plexus in mediating parasympathetic control of ventricular contractility.
  • To determine if the CMV ganglion plexus selectively influences contractility independently of heart rate and atrioventricular (AV) conduction.
  • To identify the specific neural structures responsible for vagally-induced negative inotropy.

Related Experiment Videos

Main Methods:

  • Measurements of sinus rate, AV conduction, and left ventricular contractility (LV dP/dt) in anesthetized dogs.
  • Bilateral cervical vagus nerve stimulation before and after pharmacological blockade.
  • Selective blockade of the CMV ganglion plexus using trimethaphan injection into the associated fat pad.
  • Comparison of effects with systemic or local administration of trimethaphan to other cardiac fat pads.

Main Results:

  • Vagal stimulation significantly decreased ventricular contractility (negative inotropy) and slowed sinus rate and AV conduction.
  • Blockade of the CMV ganglion plexus abolished the vagally-induced decrease in ventricular contractility.
  • CMV ganglion plexus blockade did not affect vagally-mediated sinus bradycardia or AV block.
  • Reversibility of blockade and lack of effect from trimethaphan at other sites confirmed CMV specificity.

Conclusions:

  • Parasympathetic ganglia within the CMV fat pad are critical for mediating vagally-induced negative inotropy.
  • The CMV ganglion plexus exerts selective control over ventricular contractility, distinct from its effects on heart rate and AV conduction.
  • These findings highlight the importance of localized neural circuits in fine-tuning cardiac function.