Pulmonary surfactant inhibition following cardiopulmonary bypass

Abstract

Following cardiopulmonary bypass (CPB) patients exhibit varying amounts of pulmonary dysfunction. This study examined the possibility that plasma which leaked into the alveoli could cause a reduction in the ability of pulmonary surfactant to reach very low surface tension (surfactant inhibition). The possibility that CPB could cause an increase in any component of plasma which might inhibit surfactant function was also examined. Plasma from adult and child patients was tested. Surfactant was prepared from pig lungs. Surfactant function was measured as ability to lower surface tension on a Langmuir-Wilhelmy balance. Plasma from normals and CPB patients before and after bypass was mixed with pig surfactant and tested on the balance. The surface load of surfactant was constant while the amount of plasma was varied. -- Plasma from normals, adult patients and child patients inhibited the surfactant. Serum, fibrinogen, albumin and globulins also inhibited surfactant in this assay. The amount of inhibition was proportional to the amount of protein added. No increased inhibition was seen in post-bypass vs. pre-bypass samples in adults or children. Inhibitor(s) are present in normal plasma and do not appear to be increased by the bypass procedure. It is possible that plasma components entering airspaces through leaking lung membranes may inhibit surfactant from proper function, and may contribute to lung collapse and edema seen in the ARDS of any etiology. -- The nature of the inhibition was examined by characterization of the inhibitor and by studying models of protein-surfactant interaction on the surface balance.