Degradation of elastin in experimental elastase-induced emphysema measured by a radioimmunoassay for desmosine.

Experimental emphysema, produced by a single intratracheal injection of elastase in hamsters, progresses in severity over months. To investigate whether this progression is due to continuous elastolysis, we measured the urinary excretion of desmosine by radioimmunoassay (RIA) as a measure of elastin catabolism in vivo. Normal hamster excreted 1.6 microgram of desmosine, equivalent to a daily turnover of approximately 0.4 mg of elastin. During the first 24 hr after injection of 25 units of elastase, excretion of desmosine was increased threefold, rapidly returning to normal over several days. Desmosine excretion was normal after 6 days. Homogenates of lungs from elastase-injected hamsters were incubated in vitro, and the release of soluble desmosine was followed by RIA as a measure of the active elastase in the tissue. The method was sufficiently sensitive to detect 0.1 microgram of enzyme bound to elastin. Desmosine solubilized in vitro from lungs removed at intervals after elastase injection was 10-fold that of control at 1 hr and slightly elevated at 48 hr, but equaled control levels at 7 days. These results indicate that the late progression of elastase-induced emphysema is not accompanied by increased elastolysis.