Getting the body to fight its own heart attack
Friday - Feb 26, 2010, 02:52pm (GMT+5.5)
Washington, Feb 26 (IANS) Scientists trying to find a way to better help patients protect themselves from a heart attack are taking their cues from cardiac patients.
The work has its roots in a perplexing curiosity that physicians have long observed in their patients: When faced with a heart attack, people who have had a previous one oftentimes fare better than patients who have never had one.
Scientists have been working for 25 years to understand one reason why -- a process known as ischemic preconditioning, where a temporary restriction of blood flow somehow strengthens cardiac tissues down the road.
A group led by Paul Brookes, associate professor of anesthesiology, pharmacology and physiology, University of Rochester Medical Centre (URMC) and graduate student Andrew Wojtovich have developed new methods in the effort to track down one of the key molecular agents involved.
That molecule, known as the mitochondrial ATP-sensitive potassium channel, or mKATP, is central to ischemic preconditioning, but it has proven elusive for scientists seeking to isolate and describe it.
The Rochester team has created a new way -- faster, less expensive, and easier than current methods -- to measure the activity of mKATP. The team has also identified a molecule, known as PIP2, that can restore the channel's activity even once it has stopped working properly.
The new work is expected to provide new clues about how the channel, which is thought to be central to our heart health, is regulated in the heart.
The ultimate goal of ischemic preconditioning, of course, is not to condition the heart by purposely causing a lack of blood flow to it. Rather, scientists like Brookes hope to use their knowledge to develop a new medication or treatment to help all patients better resist heart damage should it occur.
"Preconditioning has been shown to be effective in a variety of models in the laboratory, but it hasn't made it to the clinic yet," said Brookes, according to an URMC release.
"One would want to design a drug to get the benefit of ischemic preconditioning without actually impeding blood flow in any way."
These findings were published online in the Thursday edition of Circulation Research.
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