Abstract
Myocardial infarction causes pathological changes in the autonomic nervous system, which exacerbate heart failure and predispose to fatal ventricular arrhythmias and sudden death. These changes are characterized by sympathetic activation and parasympathetic dysfunction (reduced vagal tone). Reasons for the central vagal withdrawal and, specifically, whether myocardial infarction causes changes in cardiac vagal afferent neurotransmission that then affect efferent tone, remain unknown. The objective of this study was to evaluate whether myocardial infarction causes changes in vagal neuronal afferent signaling. Using in vivo neural recordings from the inferior vagal (nodose) ganglia and immunohistochemical analyses, structural and functional alterations in vagal sensory neurons were characterized in a chronic porcine infarct model and compared with normal animals. Myocardial infarction caused an increase in the number of nociceptive neurons but a paradoxical decrease in functional nociceptive signaling. No changes in mechanosensitive neurons were observed. Notably, nociceptive neurons demonstrated an increase in GABAergic expression. Given that nociceptive signaling through the vagal ganglia increases efferent vagal tone, the results of this study suggest that a decrease in functional nociception, possibly due to an increase in expression of inhibitory neurotransmitters, may contribute to vagal withdrawal after myocardial infarction.
Highlights
The autonomic nervous system plays an important role in the regulation of cardiac function [1, 2]
Effect of Myocardial Infarction on Nodose Neurons. It is unknown if myocardial infarction (MI) is associated with phenotypical changes in the neurons of the nodose ganglia
To assess these alterations after MI, ganglia were harvested from chronically infarcted animals as previously described [5, 12], and compared to ganglia from healthy animals
Summary
The autonomic nervous system plays an important role in the regulation of cardiac function [1, 2]. Cardiac disease causes significant pathological changes in the autonomic nervous system that result in sympathovagal imbalance, as reflected by sympathetic activation and vagal withdrawal [3, 4]. Enhanced vagal drive has been shown to be anti-arrhythmic, increasing cardiac action potential duration, slowing heart rate, preventing intracellular calcium overload, and reducing ventricular tachycardia (VT) inducibility [5, 6]. In the setting of myocardial injury, progressive vagal efferent dysfunction occurs, as reflected in noninvasive markers such as decreased heart rate variability. These changes are associated with an increased risk of ventricular arrhythmias in patients with myocardial infarction (MI) and increased mortality in heart failure [7, 8]. The mechanisms underlying parasympathetic dysfunction and vagal withdrawal remain unclear
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