A quest to improve treatment of lung disease

January 23, 2012 5:45 AM

Kathryn Hobgood Ray

For 250,000 patients in the U.S. suffering from acute respiratory distress syndrome (ARDS), mechanical ventilation is a necessary part of treatment. But the life-saving treatment also can cause great damage to the lungs. Tulane researchers Donald Gaver and Will Glindmeyer are investigating a new strategy that could improve the outcomes for ARDS patients.

Treating ARDS

Treatment for acute respiratory distress syndrome has come a long way since the era of the iron lung, but Tulane researchers Donald Gaver, left, and Will Glindmeyer hope to see greater improvement in mortality rates. (Photo by Paula Burch-Celentano)

“In the same way an overinflated balloon will burst, alveoli inside the lung can burst when too much air inflates them,” says Gaver, professor of biomedical engineering at Tulane. “And if too little air gets to the lungs, airways collapse and reopen and the steady repetition can inflame and swell tissues.”

Additionally, explains Gaver, ARDS can destroy surfactant, a chemical substance in the lungs that keeps lung walls from sticking together and makes lung inflation possible. The destruction of surfactant can be exacerbated by mechanical lung ventilation.  

“The challenge is ventilating someone without increasing damage to their lung, and allowing their lung to naturally heal,” says Gaver. “It’s not well known how to do this.”

While ARDS mortality rates have diminished from 90 percent in the 1940s and 1950s — the era of the iron lung — to 30 percent, improvements have leveled off.

Gaver and doctoral student Will Glindmeyer hope to jumpstart a paradigm shift in lung ventilation strategy that could further reduce ARDS mortality. They are investigating how “unconventional” breaths of air can improve surfactant function during mechanical ventilation, leading to a 50 percent reduction in cell damage.

“We use computational and experimental models to demonstrate that a dynamic flow pattern can improve surfactant function and protect sensitive pulmonary tissue,” says Gaver. The models were performed by doctoral students Jerina Pillert and Bradford Smith and research professor Eiichiro Yamaguchi.

Their research and an editorial about their work appears in the January issue of the Journal of Applied Physiology.

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