Modeling and Analysis of Central and Peripheral Autonomic Contributions to Decreased Cardiac Vagal Tone Following Myocardial Infarction

Abstract

Loss of cardiac function following myocardial infarction is accompanied by neural adaptation in baroreflex systems that are compensatory in the short term but then become associated with long-term disease progression. A hallmark of these baroreflex changes is decreased vagal tone. The closed-loop feedback structure of the baroreflexes confounds the source of decreased vagal tone following myocardial infarction (MI). We recognize that in a feedback network causality is distributed in the network interactions, and so explore the effects of MI on the potential contribution to vagal withdrawal of each neural component of our previously published closed-loop baroreflex computational model. The model is composed of differential equations representing the blood flow through various body compartments and sigmoidal functions to represent the saturating firing behavior of neurons. Neuronal adaptations leading to decreased vagal activity could occur in various neuronal groups located centrally in the brainstem. Adaptations could also occur peripherally at the baroreceptors or the heart’s “little brain”, the intrinsic cardiac nervous system. We developed five alternative models to reflect these hypotheses. Of the alternative models, only the model representing adaptation in the baroreceptors predicted both physiological baroreflex function and a decrease in vagus nerve activity. These findings suggest that decreased vagal activity after myocardial ischemia may be due, at least in part, to a decrease in baroreceptor sensitivity. We also link these model predictions with experimental evidence from the literature. NIH U01-HL133360, NIH OT2-OD030534, NSF 1940700, and NSF OAC-1919839. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.