Sleep apnea increases risk of heart diseaseMay 5th, 2009 - 2:37 pm ICT by IANS
Washington, May 5 (IANS) Obstructive sleep apnea - or periodic interruptions in breathing throughout the night - heightens risk of heart and vascular disease, besides thickening the patient’s blood vessels, says a new study.
Researchers at Emory University School of Medicine (EUSM) have identified the enzyme NADPH oxidase as important for the effects obstructive sleep apnea (OSA) has on blood vessels in the lung.
OSA affects one in every 50 women and one in every 25 men in the US. Standard treatment involves a mechanical application of air pressure.
Anything that blunts sleep apnea’s effects on blood vessel physiology could reduce its impact on disease risk, said C. Michael Hart, professor of medicine at EUSM and study co-author.
Cyclically depriving mice of oxygen - researchers call this “chronic intermittent hypoxia” (CIH) - in a way that simulates OSA gives them pulmonary hypertension.
Pulmonary hypertension, which can be life threatening, is a condition in which the right side of the heart has trouble pumping blood because of resistance in the lung’s blood vessels.
CIH forces the blood vessels in the lung to make more NADPH oxidase, Hart and his colleagues found. Mice that lack NADPH oxidase are immune to oxygen deprivation’s effects.
NADPH oxidase is a helpful enzyme because it is responsible for making superoxide, a reactive free radical that the immune system uses to kill bacteria. But superoxide also interferes with nitric oxide, a signal that allows blood vessels to relax.
Humans with mutations in genes for NADPH oxidase have recurrent bacterial infections because their ability to fight the bacteria is weakened.
Thus Hart says inhibiting the NADPH oxidase enzyme in the entire body may be harmful, and he favours an indirect intervention.
“We think that strategies to lower NADPH oxidase expression induced by hypoxia may be useful in preventing hypoxia-induced pulmonary hypertension,” says Hart.
The research was funded by the National Institutes of Health and the Veterans Affairs Research Service, said an EUSM release.
The results were published in the May issue of the American Journal of Respiratory Cell and Molecular Biology.
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