Glycocalyx Degradation after Pulmonary Transplantation Surgery

Area of Science:

• Cardiovascular Medicine
• Surgical Innovation
• Pulmonary Medicine

Background:

• Ischaemia-reperfusion injury (IRI) is a significant cause of morbidity following pulmonary resection.
• Glycocalyx degradation is implicated in endothelial dysfunction during IRI.
• Lidocaine's anti-inflammatory effects are known, but its impact on glycocalyx is unstudied.

Purpose of the Study:

• To investigate the role of the glycocalyx in lung IRI using a lung auto-transplantation model.
• To evaluate the potential of lidocaine to mitigate lung IRI by modulating the glycocalyx.

Main Methods:

• A lung auto-transplantation model was used in pigs (sham, control, lidocaine groups).
• Lidocaine was administered intravenously (1.5 mg/kg/h) to the treatment group.
• Lung tissue and plasma were analyzed for pulmonary edema, glycocalyx components (syndecan-1, heparan sulfate), adhesion molecules, and myeloperoxidase.

Main Results:

• IRI led to pulmonary edema and glycocalyx degradation, evidenced by decreased lung syndecan-1/heparan sulfate and increased plasma levels.
• Reperfusion increased neutrophil activation and adhesion molecule expression.
• Lidocaine administration significantly reduced these IRI-induced alterations.

Conclusions:

• Lung IRI involves glycocalyx degradation, contributing to neutrophil activation and adhesion.
• Lidocaine effectively protects the lung against IRI by preserving glycocalyx integrity.