Background: Alveolar type-II(ATII)-cells are exposed to mechanical stretch during breathing and mechanical ventilation. Increased stretch may contribute to lung injury.
Methods: The influence of three stretching patterns (characterized by frequency [min (-1)] - increase in surface area [%]: S40 - 13, S60 - 13, S40 - 30) on parameters of apoptosis, necrosis and membrane integrity in rat ATII cells was compared with that in static cultures. The S40 - 13 stretching pattern simulated normal breathing. The other patterns were chosen to study increased amplitude and frequency.
Results: There were no significant differences between the S40 - 13 group and static cultures. LDH release and early apoptotic cells were significantly increased in S60 - 13 and S40 - 30 in comparison with static cultures (LDH: 0.089 +/- 0.014 microg/ml and 0.177 +/- 0.050 microg/ml versus 0.050 +/- 0.011 microg/ml; early apoptosis: 17 +/- 3.5 % and 23 +/- 3.1 % versus 9.7 +/- 1.4 %) at 24 h. Necrosis was significantly increased only in the S40-30 group (13 +/- 2.4 % versus 6.1 +/- 0.9 % in static culture at 24 h). Captopril as well as L-Arginine prevented apoptosis and reduced apoptotic cells to static culture levels in the S40 - 30 group but did not influence necrosis and LDH release.
Conclusion: Increased mechanical stretch may contribute to lung injury by induction of apoptosis and necrosis in ATII cells. Apoptosis induced by high amplitude mechanical stretch is prevented by captopril and L-Arginine.