Acute respiratory distress syndrome can be caused by a number of underlying conditions, including smoke inhalation, a severe blow to the chest, bad pneumonia, septic shock, severe blood loss, or drug overdose. Although the causes vary greatly, the situation for a patient who arrives at an emergency room with acute respiratory distress syndrome is largely the same--critical. Adult respiratory distress syndrome leads to the filling of the lung's airways with fluids, a condition known as pulmonary edema. This leads to a reduction of oxygen intake, which can rapidly degenerate into complete respiratory failure.
"It's a serious complication that often results in death," says Professor Hugh Rosen, M.D., Ph.D., of The Scripps Research Institute.
Adult respiratory distress syndrome is usually treated by ventilation that increases the oxygen available to the lungs, as well as by antibiotics, muscle relaxers, pain relievers, heart stimulants, and other drugs that address some of the related problems. According to the U.S. National Heart, Blood, and Lung Institute, these therapies have helped greatly. While in the past fewer than half of all people who developed acute respiratory distress syndrome survived, now as many as seven out of ten receiving critical care in a hospital do.
Now, hoping to improve matters further, Rosen and his Scripps Research colleagues are reporting a new molecular mechanism that controls how the lungs are kept dry and under what conditions they permit fluids to enter. The mechanism involves a protein called the SIP3 receptor expressed on the surface of the cells lining the lung's air sacs. When the receptor is activated, the lungs become lea
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