Stopping Nitric Oxide Build

February 03, 1997

A drug that stops overproduction of nitric oxide, a chemical normally involved in many body functions, may reduce the risk of brain damage that sometimes occurs when the body is cooled during heart surgery, a Johns Hopkins animal study suggests.

Results show that apoptosis -- the self-destruction of cells -- is widespread in hypothermic circulatory arrest and that an excess of nitric oxide plays a significant role in brain cell damage that occurs in some cardiac pulmonary bypass patients. In hypothermic circulatory arrest, the body temperature is lowered to reduce the need for oxygen, the heart is stopped and a heart-lung bypass machine takes over circulation in an effort to prevent brain damage and give surgeons more operating time. Prolonged hypothermic circulatory arrest, however, may increase the risk of brain damage, such as learning and memory problems and involuntary movements.

"Our findings suggest that strategies to protect the brain during hypothermic circulatory arrest may include preventing runaway production of nitric oxide," says Elaine E. Tseng, M.D., the study's lead author and a surgery fellow. Results will be presented Feb.3 at the Society of Thoracic Surgeons' annual meeting in San Diego.

After 14 dogs underwent bypass surgery and two hours of hypothermic circulatory arrest, the seven dogs treated with the drug 7-nitroindazole showed decreased nitric oxide in the brain and significantly less apoptotic brain cell damage than the seven untreated dogs, the results show. The drug works by inhibiting the enzyme that makes nitric oxide, which has an important role in regulating blood pressure, transmitting messages between nerve cells and other functions.

Johns Hopkins Medicine

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