Activation of persistent Na+ current during hypoxia: oxygen sensors, Na+ channel subunits and drugs.

Funded Activity Summary

Cardiac arrhythmias (a variation in the normal rhythm of a heart beat) and stroke are a major causes of sudden death in industrialised countries. Stroke is the second greatest killer in Australia, claiming 12, 133 lives in 1997. It is also the leading cause of long term disability in adults, costing ~$630 million-year. Both stroke and arrhythmias are often caused by occlusion (closure or blockage) of arteries which deprives the brain or the heart of oxygen (hypoxia). Clinicians and pharmaceutical companies are very aware of the need for better treatments for these disorders. While we understand some of the cellular changes and events that take place when a cell is deprived of oxygen, we lack the precise knowledge of the critical timing and the sequence of events that eventually lead to cell damage and death. It can be appreciated that this knowledge would greatly aid the development of new drug treatments. The market for new drugs to prevent cell damage during heart attack and stroke has been estimated at ~$2 billion. This project has great clinical significance since we are looking at inhibiting the cascade set in motion by hypoxia at an early stage via a persistent sodium current. We believe this will give better and more effective treatments than are currently available.

Funded Activity Details

Start Date: 01-01-2002

End Date: 01-01-2004

Funding Scheme: NHMRC Project Grants

Funding Amount: $338,820.00

Funder: National Health and Medical Research Council

Research Topics

ANZSRC Field of Research (FoR)

Medical biotechnology diagnostics (incl. biosensors)

ANZSRC Socio-Economic Objective (SEO)

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Other Keywords

anoxic cell damage | arrhythmias | cardiac/cerebral ischaemia | cardiovascular disease | electrophysiology | hypoxia | molecular biology | patch clamp | sodium channel | stroke and heart attack

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