Adrian H. Chester

Early Detection of Lung Endothelial Dysfunction in Man

Pulmonary vascular endothelial cells express a variety of transporter and enzyme proteins which are known or suspected modulators of cardiovascular homeostasis and are susceptible to injury (Ryan, U.S., 1987). Over the past decade, studies by us and other investigators have accumulated considerable experimental evidence suggesting that the activity of pulmonary capillary endothelium-bound angiotensin converting enzyme (ACE), a prominent endothelial ectoenzyme which is uniformly distributed throughout the vasculature, can be assayed repeatedly, accurately and reproducibly, in vivo (Ryan, J. W., 1977, 1991; Catravas et alt 1981, 1983). Reduced endothelium-bound ACE activity is the earliest yet known manifestation of impeding lung injury in various animal models of lung damage, in vivo (e.g., hyperoxia, irradiation, bleomycin, activated neutrophil, etc.) (Bakhle, 1979; Catravas et al, 1984, 1989; Gillisetal, 1986; McCormick etal, 1987; Tovvonen etal, 1981). Based on these findings, we have hypothesized that monitoring of changes in pulmonary capillary endothelium-bound ACE activity may be used as a diagnostic test to aid in the early detection of lung injury in man.