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Related Concept Videos

Regulation of Heart Rates01:31

Regulation of Heart Rates

The regulation of heart rate is a complex process controlled by the autonomic nervous system (ANS), hormonal influences, and intrinsic cardiac mechanisms. The ANS has two main components: the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS).
The SNS increases heart rate through the release of norepinephrine and epinephrine, which act on beta-1 adrenergic receptors in the heart. This action increases the rate of depolarization in the sinoatrial (SA) node, the heart's...
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The heart rate, or pulse rate, is a vital indicator of cardiovascular health. It reflects the number of times the heart beats per minute. Various physiological and environmental factors influence heart rate, increasing or decreasing cardiac output. Understanding these factors is crucial for assessing heart function and identifying potential health issues.
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Sympathetic Activation01:16

Sympathetic Activation

The sympathetic division can influence tissues and organs by releasing norepinephrine at peripheral synapses and distributing epinephrine and norepinephrine through the bloodstream. In times of crisis or stress, sympathetic activation occurs, which is regulated by sympathetic centers in the hypothalamus. As a result, sympathetic activation prepares the body for physical exertion, rapid ATP production, and heightened alertness, allowing individuals to respond effectively to challenging or...
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Disorders of the Autonomic Nervous System

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G-Protein Gated Ion Channels01:21

G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
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Pathogen-induced heart rate changes associated with cholinergic nervous system activation.

Karen D Fairchild1, Varadamurthy Srinivasan, J Randall Moorman

  • 1Dept. of Pediatrics, University of Virginia Health System, Hospital Dr., Charlottesville, VA 22908, USA.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|November 12, 2010
PubMed
Summary

Sepsis triggers a paradoxical vagal response, causing transient heart rate slowing and increased variability, followed by decreased variability, cytokine release, and mortality. This highlights the complex role of the vagus nerve in sepsis.

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Area of Science:

  • Neuroimmunology
  • Autonomic Nervous System Physiology
  • Sepsis Pathophysiology

Background:

  • The autonomic nervous system regulates host defense and sepsis responses, including heart rate variability (HRV).
  • The cholinergic anti-inflammatory pathway predicts increased vagal signaling and HRV in sepsis, contrasting with observed decreased HRV.
  • A paradox exists between predicted and observed HRV changes in sepsis, necessitating further investigation into vagal nerve involvement.

Purpose of the Study:

  • To elucidate the role of the vagus nerve in sepsis-induced heart rate variability changes.
  • To investigate the mechanisms underlying transient bradycardia and subsequent HRV alterations during infection.
  • To explore the desensitization of the vagal response to pathogens in sepsis.

Main Methods:

  • Induction of sepsis in mice via intraperitoneal injection of bacteria or Candida albicans.
  • Assessment of heart rate, heart rate variability, and bradyarrhythmias.
  • Pharmacological blockade of muscarinic cholinergic receptors with atropine.
  • Evaluation of vagal afferent signaling using c-Fos activity.
  • Analysis of plasma cytokine levels and mortality rates.

Main Results:

  • Pathogen injection rapidly induced bradyarrhythmias and transiently increased short-term HRV, indicating vagal efferent activity.
  • Atropine terminated pathogen-induced bradycardias, confirming the role of vagal signaling.
  • Vagal afferent signaling was evident in the vagal sensory ganglia and brain stem.
  • Pathogen-induced bradycardia showed rapid desensitization upon repeat exposure.
  • Following initial recovery, some mice developed depressed HRV, correlated with elevated cytokines and mortality.

Conclusions:

  • The vagus nerve mediates transient cardiac deceleration and increased HRV during early sepsis, followed by desensitization.
  • Decreased HRV in later sepsis stages is linked to cytokine release, mortality, and desensitization of the vagal response.
  • These findings reconcile the paradox of increased and decreased HRV in sepsis, offering insights into sepsis pathophysiology and potential therapeutic targets.