"And if you were born with very few, the last thing you would want to do is subject yourself to environmental factors that might further cut down the number of these vessels." Faber also is a member of the McAllister Heart Institute at UNC. Earlier this year, his team reported that these vessels form early in life and that genetic background has a major impact on how many you end up with.
The factors that put people at risk for developing stroke, heart attack, or peripheral artery disease include the usual suspects -- smoking, diabetes, hypertension, high cholesterol, family history, age. But until recently, researchers didn't know what linked those risk factors together, when it comes to insufficiency of the collateral circulation.
Faber says studies have shown that all of these factors cause the endothelial cells that line our blood vessels to produce less nitric oxide, a "wonder molecule" that protects our vasculature from disease. Now, he says, his group's findings indicate that this molecule is also a critical factor maintaining the health of the collateral circulation.
So Faber and lead study author Xuming Dai, M.D., Ph.D., of UNC's departments of medicine and physiology, wondered whether collateral vessels would be lost if the levels of nitric oxide were suppressed. They counted the number of these vessels in the brains of mice genetically engineered to lack the enzyme called eNOS -- that makes most of the nitric oxide in blood vessel walls.
The researchers found that from the ages of three months to six months (equivalent to about twenty-one to forty-five years of age in humans) there was a 25 percent reduction in the number of collateral vessels in the mutant mice as compared to normal ones. They also saw the same percentage decrease in collateral vessels supplying the legs, where they were trying t
|Contact: Les Lang|
University of North Carolina School of Medicine