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Atherosclerosis May Also Harm Vital Organs
Toxic byproduct of plaque formation wreaks havoc on heart, lungs and liver, study suggests
By Theresa Waldron
HealthDay Reporter
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THURSDAY, April 10 (HealthDay News) -- New research indicates that the fatty plaques that harden arteries may also harm vital organs.
"Atherosclerosis is usually associated with plaque formation in arteries," said study author Rita K. Upmacis, an associate research professor in pathology and laboratory medicine at Weill Medical College of Cornell University in New York City. "But using a mouse model of atherosclerosis, we have demonstrated that the effects of this disease are more widespread, affecting . . . the heart, liver and lungs."
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The finding, scheduled to be presented this week at the American Chemical Society annual meeting, in New Orleans, centers around the availability of nitric oxide (NO), an important gas within the body that relaxes blood vessel walls and helps prevent atherosclerosis. Certain substances in plaque remove NO and create a toxic substance known as peroxynitrite, which hampers the function of enzymes necessary to the health of blood vessel walls.
In the latest study, researchers found that in mice that were fed a high-fat diet and who developed atherosclerosis, peroxynitrite, nitrotyrosine and other substances that interfered with NO were common not only in the blood vessels, but also in the hearts, lungs and liver.
"During many disease states, reactive oxygen species such as superoxide are formed," explained Upmacis. "The problem here is that nitric oxide, which is beneficial to the body, reacts with superoxide, and forms something called peroxynitrite, which is a powerful oxidant that can cause all sorts of damage and wreak havoc. These reactions are predicted to lead to the vascular dysfunction encountered in atherosclerosis."
It is possible drugs could be developed to increase NO production and prevent organ damage from atherosclerosis. However, there could be unwanted side effects, such as an increased risk of infection, so it would be difficult to create a drug targeted specifically to atherosclerosis, Upmacis said.
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Copyright © 2008 ScoutNews, LLC. All rights reserved.
Last updated 4/10/2008
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SOURCES: John C. LaRosa, M.D., president, State University of New York Downstate Medical Center, New York City; Alan Kadish, M.D., associate director, Northwestern Cardiovascular Institute, Chicago; Rita K. Upmacis, Ph.D., associate research professor, pathology and laboratory medicine, Weill Medical College of Cornell University, New York City; April 9, 2008, presentation, American Chemical Society annual meeting, New Orleans
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