Apoptosis and Necrosis Induced by Cyclic Mechanical Stretching in Alveolar Type II Cells

• DOI: 10.1165/rcmb.2003-0136oc
• Publication Date: 2003-09-09T02:31:13Z
• Authors: Stefan Hammerschmidt; Hartmut Kuhn; Thomas Grasenack; Christian Gessner; Hubert Wirtz
• Keywords: Male; 0301 basic medicine; Caspase 8; Captopril; Angiotensin II; Apoptosis; Arginine; Rats; Pulmonary Alveoli; Rats, Sprague-Dawley; Necrosis; 03 medical and health sciences; Caspases; Animals; Stress, Mechanical; Annexin A5; Lactate Dehydrogenases; Antihypertensive Agents

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