Activated polymorphonuclear(PMN) leukocyte may cause lung injury by peroxidation and proteolysis in adult respiratory distress syndrome(ARDS). Recently, Liau et al.(Biochim Biophy Acta, 1996) reported that PMN elastase may inactivate pulmonary surfactant(PS) by proteolytic degradation of surfactant protein. Authors reported previously H2O2 inactivated PS (Pediatr Res(A), 1997). However, it is unclear that PMN myeloperoxidase, which is a source of H2O2, may inactivate PS. We hypothesized that surface active properties(SAP) of PS would be compromised by addition of PMN myeloperoxidase® (MPX, Sigma chemical, St. Louis) and PMN Elastase® (ELA, Sigma chemical, St. Louis). To prove this, we prepared mixtures with Surfacten® (S-TA, Tokyo Tanabe, Japan) + MPX and S-TA + ELA. Pulsating Bubble Surfactometer (Electronetics, NY) was used to measure in vitro minimum and maximum surface tensions(ST) and area-surface tension relationship. Results are 1) S-TA and 5U MPX were mixed to the final concentrations of S-TA 0.5 mg phospholipids/ml, and incubated at 37¡É for 24 hour. The maximum and minimum ST after 5 min of pulsation increased significantly and area-surface tension was lost. 2) When 1U ELA was added to S-TA, the results were similar to that of MPX.

In conclusion, The addition of leukocyte MPX and ELA to PS could interfere with SAP of PS. Therefore, we suggest that in the pathogenesis of ARDS, leukocyte enzyme as well as leukocyte itself affect SAP of PS. Table

Table 1 No caption available.
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