| Περίληψη: | The nervous system maintains physiological homeostasis through reflex pathways that modulate organ function. This process begins when changes in the internal milieu (e.g., blood pressure, temperature, or pH) activate visceral sensory neurons that transmit action potentials along the vagus nerve, the longest nerve of the autonomic nervous system, to the brainstem. IL-1β and TNF, inflammatory cytokines produced by immune cells during infection and injury, and other inflammatory mediators have been implicated in activating sensory action potentials in the vagus nerve. The extraction of metrics that describe the functioning of the cardiovascular system, as well as its general modeling, is an important factor in understanding the human body, as well as in predicting future situations. Heart rate Variability (HRV) has been suggested by many studies to work as a proxy for many conditions and one of them is the inflammation. Here we employ methods to process cardiac and vagus nerve biosignals, extract HRV measurements and model the relationship between them to infer if the cytokine-specific information in sensory neural signals within the vagus nerve is also present in the HRV. Firing rates of the vagus nerve of mice responders to IL-1β and TNF exposure and saline exposure as a control, as well as heart activity from the nerve recordings were used for the study. A plethora of HRV measurements were extracted and their statistical properties were examined for the different states. The measurements that were statistically significant were the RMSSD (P < .05), SDSD (P < .05), SD1 (P < .05) and SD1nu (P < .05) for the case of TNF. For the modeling of the relationship ARMAX models were fitted but were not able to denote a noteworthy behavior. However, it can be challenged that a relationship is emerging between HRV and the vagus nerve activity in inflammation.
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