Cardiac arrhythmias and cardiac contractility during stress: regulation by brainstem medullary raph neurons

Funding Activity

Website
http://purl.org/au-research/grants/nhmrc/324736

Funding Status
Closed

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Funded Activity Summary

Life is stressful, and in subjects with predisposed hearts stressful events may provoke sudden life-threatening or fatal disturbances of the heart rhythm (arrhythmias). Activity in nerves that control the heart is the main trigger of arrhythmias. This activity is initiated in the brain, when, for example, we have a sudden emotional shock. At present, the neurochemistry and connections of the brain neurons responsible for arrhythmias, have not been identified. Our project is designed to find answers to these questions. Our hypothesis is that the responsible neurons are located in the midline portion of the medulla oblongata (the lower part of the brain); that activation of these neurons will increase cardiac function in a manner that may provoke arrhythmias; and, conversely, that their inhibition will protect the heart during stressful events by suppressing potentially arrhythmogenic neural signals. We hypothesise that cardiac-controlling neurons possess receptors for serotonin (one of the brain neurotransmitters), and that the neurons can be inhibited by drugs that selectively activate a specific subtype of these receptors. Our results will increase our understanding of the causes of cardiac arrhythmias by elucidating the link between emotional-psychological events in the brain and stress-induced cardiac events. Our findings could contribute to the identification of new drugs that will protect the heart during stress.

Funded Activity Details

Start Date: 01-01-2005

End Date: 01-01-2007

Funding Scheme: NHMRC Project Grants

Funding Amount: $425,250.00

Funder: National Health and Medical Research Council

Research Topics

ANZSRC Field of Research (FoR)

Cardiology (incl. Cardiovascular Diseases)

ANZSRC Socio-Economic Objective (SEO)

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Other Keywords

arrhythmia | arrhythmogenesis and sudden death | electrophysiological measures | myocardial contractility | stress | stress response | sudden cardiac death | ventricular tachycardia

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