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Johns Hopkins Medicine
Office of Corporate Communications
MEDIA CONTACT: David March
November 10, 2004
WALLFLOWER BIOCHEMICAL PATHWAY HAS PROTECTIVE ROLE IN HEART FAILURE
For more than a decade, nitric oxide-making enzymes have been recognized as key players in protecting the heart from further damage after a heart attack, but new research from Johns Hopkins reveals that the least well-studied of the three enzymes could be the most important in the heart.
Most research has focused on the first two versions of the enzyme found in the heart: inducible and endothelial nitric oxide synthase. Now, in animal studies, researchers at Johns Hopkins have confirmed a greater protective role for the last enzyme found, constitutive nitric oxide synthase, also known as myocyte neuronal nitric oxide synthase (NOS1) because of its consistent presence in heart and brain cells.
Nitric oxide plays a critical role in recovery from a heart attack: It can dilate, or expand, the coronary arteries, and help regulate the strength of the hearts contraction, said cardiologist Roberto Saraiva, M.D., a research fellow at The Johns Hopkins University School of Medicine and its Heart Institute. Now we know that myocyte neuronal nitric oxide synthase, specifically, increases survival rates and heart function in mice after heart attack. Next, we have to figure out why and, possibly, attempt to harness these benefits as a future therapy.
Mice without the NOS1 gene were 2.5 times more likely to die within 60 days after a heart attack compared to mice with the gene. Indeed, cardiac function was 20 percent worse in the mice without the NOS1 than in the control group.
Neuronal Nitric Oxide Synthase Deficient Mice Have Increased Mortality and Depressed Cardiac Performance Following Myocardial Infarction. Roberto Saraiva, Cheuk Sun, Khalid Minhas, Daniel Durand, Koenraad Vandegaer, Lili Barouch and Joshua Hare.
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(Abstract Oral Sessions #1603, Room 398-399, Ernest N. Morial Convention Center.)