Our results suggest that lidocaine can prevent OLV-induced lung injury through reduced expression of proinflammatory cytokines and lung apoptosis. Administration of lidocaine may help to prevent lung injury during lung surgery with OLV.

No abstract

Purpose: Ischaemia-reperfusion injury (IRI) is a main cause of morbidity after pulmonary resection surgery. The degradation of glycocalyx, a dynamic layer of macromolecules at the luminal surface of the endothelium, seems to participate in tissue dysfunction after IRI. Lidocaine has a proven anti-inflammatory activity in several tissues but its modulation of glycocalyx has not been investigated. This work aimed to investigate the potential involvement of glycocalyx in lung IRI in a lung auto-transplantation model and the possible effect of lidocaine in modulating IRI. Methods: Three groups (sham-operated, control, and lidocaine), each consisting of 6 Large White pigs, were subjected to lung auto-transplantation. All groups received the same anaesthesia. In addition, the lidocaine group received a continuous IV administration of lidocaine (1.5 mg/kg/h). Lung tissue and plasma samples were taken before pulmonary artery clamp, before reperfusion, and 30 and 60 min post-reperfusion in order to analyse pulmonary oedema, glycocalyx components, adhesion molecules, and myeloperoxidase level. Results: Ischaemia caused pulmonary oedema, which was greater after reperfusion. This effect was accompanied by decreased levels of syndecan-1 and heparan sulphate in the lung samples, together with increased levels of both glycocalyx components in the plasma samples. After reperfusion, neutrophil activation and the expression of adhesion molecules were increased. All these alterations were significantly lower or absent in the lidocaine group. Conclusion: Lung IRI caused glycocalyx degradation that contributed to neutrophil activation and adhesion. The administration of lidocaine was able to protect the lung from glycocalyx degradation.

Surgical manipulation of the collapsed lung could increase the expression of inflammation and proapoptotic mediators and cause tissue damage in the form of pulmonary oedema. Sevoflurane could attenuate this molecular response and pulmonary oedema.

No abstract