School of Medicine and Health Sciences Poster Presentations

Title

Effect of Oxytocin on Obstructive Sleep Apnea and Heart Failure

Poster Number

143

Document Type

Poster

Status

Medical Student

Abstract Category

Cardiology/Cardiovascular Research

Keywords

Oxytocin, obstructive sleep apnea, heart failure

Publication Date

Spring 2018

Abstract

As many as 24% of males and 9% of females within the United States population suffer from obstructive sleep apnea (OSA), which poses significant cardiovascular risks, including sudden death, hypertension, arrhythmias, myocardial ischemia, and stroke. Yet, the primary treatment for OSA, continuous positive airway pressure (CPAP), is poorly tolerated by patients and has a low compliance rate of 50-60%. Intermittent hypoxia and arousals from OSA lead to perturbations of the autonomic nervous system. Such increase in sympathetic activity and decrease in parasympathetic activity are partly responsible for the adverse cardiorespiratory events associated with OSA. Recent studies have shown that activating oxytocin receptors correct the autonomic imbalance in fight-or-flight situations. Therefore, we tested whether or not intranasal oxytocin administration can prevent or reverse adverse cardiorespiratory events by increasing parasympathetic activity and restoring the autonomic balance during apneic and hypopneic events. We saw no statistically significant difference in arrhythmia frequencies between the oxytocin treatment night and the placebo night. However, since the subjects recruited for the study did not have pre-existing heart conditions, it is possible that arrhythmias were too infrequent and random for comparison.

Similar to OSA, heart failure (HF) is marked by an autonomic imbalance: increased sympathetic activity and parasympathetic withdrawal. Although beta blockers, common medication prescribed to HF patients, are able to control the elevated sympathetic activity, it does not address the reduction in cardiac parasympathetic tone associated with HF. Recent animal studies show that increasing parasympathetic tone during HF via vagal nerve stimulation improved left ventricular structure and function. Therefore, we assessed oxytocin neuron activation as a means to improve cardiac function in an animal model of HF. Oxytocin neuron activation did not significantly change arrhythmia frequency. We observed possible ST segment changes, which needs to be further investigated. Oxytocin remains a potential therapeutic agent for OSA and HF, but additional work is needed to optimize its course in treatment.

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Effect of Oxytocin on Obstructive Sleep Apnea and Heart Failure

As many as 24% of males and 9% of females within the United States population suffer from obstructive sleep apnea (OSA), which poses significant cardiovascular risks, including sudden death, hypertension, arrhythmias, myocardial ischemia, and stroke. Yet, the primary treatment for OSA, continuous positive airway pressure (CPAP), is poorly tolerated by patients and has a low compliance rate of 50-60%. Intermittent hypoxia and arousals from OSA lead to perturbations of the autonomic nervous system. Such increase in sympathetic activity and decrease in parasympathetic activity are partly responsible for the adverse cardiorespiratory events associated with OSA. Recent studies have shown that activating oxytocin receptors correct the autonomic imbalance in fight-or-flight situations. Therefore, we tested whether or not intranasal oxytocin administration can prevent or reverse adverse cardiorespiratory events by increasing parasympathetic activity and restoring the autonomic balance during apneic and hypopneic events. We saw no statistically significant difference in arrhythmia frequencies between the oxytocin treatment night and the placebo night. However, since the subjects recruited for the study did not have pre-existing heart conditions, it is possible that arrhythmias were too infrequent and random for comparison.

Similar to OSA, heart failure (HF) is marked by an autonomic imbalance: increased sympathetic activity and parasympathetic withdrawal. Although beta blockers, common medication prescribed to HF patients, are able to control the elevated sympathetic activity, it does not address the reduction in cardiac parasympathetic tone associated with HF. Recent animal studies show that increasing parasympathetic tone during HF via vagal nerve stimulation improved left ventricular structure and function. Therefore, we assessed oxytocin neuron activation as a means to improve cardiac function in an animal model of HF. Oxytocin neuron activation did not significantly change arrhythmia frequency. We observed possible ST segment changes, which needs to be further investigated. Oxytocin remains a potential therapeutic agent for OSA and HF, but additional work is needed to optimize its course in treatment.