Type-II pneumocytes secrete pulmonary surfactant via exocytosis of lamellar bodies in order to maintain a low alveolar surface tension. An important stimulus by which the surfactant exocytosis can be triggered is a deep inflation of the lung, however it is yet unknown to which type of stretch pneumocytes respond most. Equibiaxial stretch has already been shown to lead to Ca2+ entry and lamellar bodies fusion.Here, we applied uni-axial strain to rat pulmonary type II cells in primary culture. For this purpose we seeded the isolated type II pneumocytes on silastic membranes and applied a 20% and 40% increase in membrane length two days later. Lamellar body fusion with the plasma membrane was detected by fluorescence microscopy using the amphiphilic dye FM 1-43. We found that type II pneumocytes react to uni-axial strain with lamellar body fusion in an amplitude-dependent manner. Furthermore, FM 1-43 can be considered as an indicator of cell membrane damage, because disruption of the plasma membrane at high strain amplitudes occasionally caused diffuse cytosolic accumulation of the dye. We conclude that uni-axial strain induces surfactant secretion at amplitudes comparable to equi-biaxial strain. At high strain amplitudes, membrane damage may occur. Supported by FWF, Projects P15742 & P15743; DFG, Project D1402 and the 6th framework of the EU, Pulmonet.