AMIODARONE-INDUCED CHANGES IN SURFACTANT PHOSPHOLIPIDS OF RAT LUNG

Amiodarone HCI (AD) is a very effective antiarrhythmic drug, but its u se is often associated with serious pulmonary complications. It is sho wn to induce lung phospholipidosis. Nevertheless, the effects of this drug on pulmonary surfactant which is composed of about 75% phospholip ids and which prevents alveolar collapse is not known. Therefore, we h ave examined the effect of AD on the intra- and extracellular surfacta nt pools and on the levels of phosphatidylcholine (PC), the primary co nstituent of pulmonary surfactant. Male Wistar rats were fed AD (175 m g/kg) by oral gavage for three weeks. At the end of the experimental p eriod, the rats were killed, the lungs removed and perfused, and surfa ctant isolated. Some lungs were prepared for ultrastructural examinati on. Phospholipid was assayed in the intra- and extracellular surfactan t. Amiodarone produced a significant increase in both the intra- and e xtracellular sufactant phospholipid along with an appreciable change i n the phospholipid profile. Also, the drug seemed to increase the numb er of lamellar inclusions in the surfactant producing type II alveolar cells. These data suggest that administration of AD leads to an incre ase in the lung surfactant phospholipid levels and lamellar bodies in alveolar type II cells.