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Research may Yield Improved Treatment for Diseased Lungs

y altering the wave patterns," says Chesler. "So a goal of this project is to investigate whether that occurs also on the right side. If it does, it'll open up all sorts of new treatment possibilities, because we haven't been treating the large arteries because we haven't been thinking of them as part of the problem."

Researchers have measured impedance, which is like resistance but takes into account arterial stiffness, in human pulmonary circulation since the 1960s. But while these measurements show that large-artery stiffening occurs, the data don't show whether that stiffness affects ventricular function, says Chesler.

She, too, will measure impedance in the pulmonary circulation, focusing specifically on the role of a particular protein, collagen, in arterial stiffening. A key innovation in molecular biology will enable Chesler to use transgenic mice to explore the physical role of collagen-mediated large-artery stiffening in pulmonary arterial hypertension. She will induce large-artery stiffness in the mice in a process that mimics scleroderma, a disease in which the body produces too much collagen, the body's ubiquitous fibrous structural protein that strengthens blood vessels.

Patients with certain kinds of scleroderma also contract a kind of pulmonary hypertension that is particularly resistant to most treatments. So in a limited series of studies in such patients, Chesler also will investigate whether excess collagen negatively affects heart health. "My hypothesis is that patients with scleroderma do particularly poorly because all this excess collagen is stiffening the large and smaller vessels," she says. "We're not addressing that with modern treatments, and so we need to look at effects of stiffness on blood flow patterns and ventricular function in this context."


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