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Heart-stopping drugs

A NEW way of stopping the heart during bypass operations could reduce damage to the heart and improve patients' chances of a full recovery.

More than a million people a year have open-heart surgery to unblockor bypass clogged arteries, or repair damaged valves. The heart is usually stopped for about one hour while they are under the knife because it is impossible to operate on a moving target. But the standard method of achieving this- flooding the heart with potassium ions- can cause permanent damage.

Now Geoffrey Dobson and Michael Jones of James Cook University in Townsville, Australia, have developed an alternative. It has only been tested on animals so far, but experts say the results, due to appear in the Journal of Thoracic and Cardiovascular Surgery, look promising. "By keeping potassium levels normal they are preventing injuries to the muscle cells and to the vessels that carry blood to the heart," says Peter Macdonald, a cardiologist at St Vincent's Hospital in Sydney.

In resting muscle cells, the distribution of ions across the cell membrane generates an electric potential. The waves of electrical activity that sweep across the heart, telling muscle cells to contract, are generated when channels in the membrane open, allowing ions to flow across the membrane and depolarise the cells. Flooding the heart with potassium ions freezes its cells in this depolarised state.

Dobson and Jones instead freeze the heart in the resting state using two drugs: adenosine, which opens some of the channels that transport potassium ions in and out of the cell, and lignocaine (known as lidocainein the US), which blocks sodium ion channels.

"There are two ways to stop a heart cell. Let it run out of gas- that's the potassium infusion-or to not even turn it on. That's what Dobson has done," says Jakob Vinten-Johansen, a cardiovascular physiologist at Emory University in Atlanta, Georgia, who now collaborates with Dobson.

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Contact: Claire Bowles
claire.bowles@rbi.co.uk
44-207-331-2751
New Scientist
17-Sep-2003


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