Objective Among the complications after cardiac surgery the development of postoperative pulmonary distress is a serious problem. Typically, the patients leave the operating theatre with good blood gas values and O 2-saturation, but develop their respiratory problems within the next hours/days. We investigated whether extracorporeal circulation may induce biochemical and histological changes in the lungs which may help to explain this development. Methods Piglets (6–10 kg) were anaesthetized using isoflurane and underwent extracorporeal circulation (ECC) with hypothermic (25–28 °C) cardioplegic arrest for 90 min followed by 3 h reperfusion. An additional group received a poly(ADP-ribose) polymerase (PARP)-Inhibitor, INO1001. Cardiopulmonary monitoring was performed during the whole procedure. Finally, lungs were explanted and investigated by histomorphometry and immunohistology for heat shock protein HSP70 (indicator for cellular damage) and TNFα in comparison to normal piglets without ECC. Results Histologically we found significant swelling of the type I alveocytes (thickness increased from 2.4 to 3.2 μm), interstitial oedema, intra-alveolar erythrocyte (4.8 versus 0.4 erythrocytes/alveole) and granulocyte accumulation and fibrinous exudates. There was a significant up-regulation of TNFα and of the cellular repair enzyme HSP70, while in control piglets only minimal levels were observed. INO1001 significantly reduced ECC-induced elevation in TNFα and in HSP70. Despite the dramatic changes after heart-lung-machine (HLM), blood gases and gas transport were almost not affected at that time. Conclusions ECC can lead to early significant histological and histochemical changes which have similarities with a beginning early stage shock lung, although – at 3 h reperfusion – gas transport is still sufficient. INO1001 can partially antagonize these changes.