PROVIDENCE, R.I. -- Good science requires great patience. In many fields, ideas and theories surge ahead while the tools to test them can take decades to catch up. When Pe-ter Richardson began talking with colleagues who were modeling blood flow through the vessels on the heart's surface, he hardly suspected that the collaboration would lead to a test of ideas he had proposed over 30 years earlier.
The resulting model, described in the online edition of Proceedings of the National Acad-emy of Sciences appearing the week of October 30-November 3, could help evaluate candidate drugs aimed at preventing blood clots a major cause of strokes, heart attacks and organ transplant rejection.
In 1970, Richardson, who had been working on the clotting problems associated with ar-tificial organs, saw a paper describing the time course of clot formation in uninjured blood vessels. Gustav Born and his co-author, Nicola Begent, had found an odd relation-ship -- shaped like a playground slide -- between the rate of blood flow and the rate of blood clot, or thrombus, formation. As blood flow increased, the rate at which the clot grew increased rapidly, up to a point. After that point, the rate of growth declined sud-denly and then gradually flattened out.
Richardson recognized that there must be two groups of processes at work -- probably one chemical and one physical. The increase in clotting with flow made sense. Faster blood flow meant more platelets encountered the clot each second, so more had a chance to be captured by it. But the decrease was puzzling.
Researchers knew that ADP (adenosine diphosphate) released from injured tissue or ex-isting thrombi could signal platelets to begin sticking together at the site of the injury. Richardson proposed that a short delay between triggering and activation could explain the decrease in aggregation with increased blood flow. "If triggering is the time when the alarm goes off" says Richardson, a
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