OP 170. Lidocaine Preserves the Endothelial Glycocalyx in a Lung Transplant Model


L. Rancan, S. Paredes, G. Cruz, G. Sánchez Pedrosa, G. Cusati, I. Garutti, C. Simón, E. Vara

Chair(s): Jiri Fronek, Mehmet Erikoglu & Mátyás Kiss

10:20 - 10:30h at Buda Room (B)

Categories: Oral Session, Organ and Cell Transplantation, Thoracic Surgery

Session: Oral Session XVIII - Organ and Cell Transplantation II


Background
Healthy vascular endothelium is coated by the glycocalyx, important in endothelial functions, but destroyed by ischaemia/reperfusion (/IR). Lidocaine is a local anesthetic which has antiinflammatory activity. The influence of lidocaine on glycocalyx structure has not been investigated. This study aimed to investigate a possible protective effect of lidocaine on lung glycocalix injury secondary to I/R injury.

Material and Methods
Two groups (lidocaine and control) of 6 pigs each were submitted to a left lung autotransplant. All groups received the same anaesthetic induction. In addition animals of lidocaine group received a continuous IV administration of lidocaine during surgery. In order to measure the levels of inflammatory (ICAM-1, VCAM-1, IL-1B, TNFx), anti-inflammatory (IL10) and glycocalix degradation (syndecan-1) markers, blood and lung tissue samples were taken: 1) 5 minutes before pulmonary artery clamp (PPn), 2) 5 min before reperfusion (PRp), 3) 30 min post-reperfusion (PR30), 4) 60 min post-reperfusion (PR60).

Results
In lung samples, levels of all inflammatory markers were markedly higher (p<0.05) at PR30 timepoint compared to PPn and PRp values. This increase was higher at PR60. I/R decreased IL10 expression. I/R increased syndecan-1 and ICAM concentrations in plasma (p<0.05). Syndecan-1 levels decreased in the lung (p<0.05). These effects were partially blocked by lidocaine.

Conclusion
These results suggest that lidocaine prevents I/R-induced glycocalyx injury in a lung autotransplant model through decreases in proinflammatory cytokines and adhesion molecules. This strategy of lidocaine administration might be a prospective management for preventing lung injury secondary to I/R.