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Ann Thorac Surg 2002;73:1101-1106
© 2002 The Society of Thoracic Surgeons

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Original article: general thoracic

The effect of adhesion molecule blockade on pulmonary reperfusion injury

^a Cardiothoracic Surgical Unit, Queen Elizabeth Hospital, Edgbaston, Birmingham, United Kingdom

* Address reprint requests to Dr Bonser, Cardiothoracic Surgical Unit, Queen Elizabeth Hospital, Edgbaston, Birmingham, B15 2TH, United Kingdom
e-mail: r.s.bonser{at}bham.ac.uk

Presented at the Poster Session of the Thirty-sixth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 31–Feb 2, 2000.

Background. Selectins are the molecules involved in the initial adhesion of the activated neutrophil on pulmonary endothelium. We investigated the efficacy of selectin blockade in a selective (monoclonal antibody RMP-1) and nonselective (Fucoidin) manner in pulmonary reperfusion injury.

Methods. Groups of six rat lungs were flushed with University of Wisconsin solution then stored at 4°C for 4 hours. They then underwent sanguinous reperfusion for 30 minutes during which functional measures (gas exchange, pulmonary artery pressure, and airway pressure) of lung performance were made. After reperfusion we estimated their capillary filtration coefficient (K_fc units g/cm water/minute/g wet lung tissue) using a gravimetric technique. Four groups were studied: group I had no reperfusion, group II had 30 minutes of reperfusion, group III had infusion of 20 mg/kg Fucoidin before reperfusion, and group IV had infusion of 20 µg/mL RMP-1 before reperfusion.

Results. Reperfusion injury was found between groups I and II by an increase in capillary filtration coefficient (1.048 ± 0.316 to 3.063 ± 0.466, p < 0.01). Groups III and IV had a significantly lower K_fc than group II (0.967 ± 0.134 and 1.205 ± 0.164, respectively, p < 0.01). There was no significant functional difference between groups II, III, and IV.

Conclusions. Reperfusion-induced hyperpermeability was ameliorated by selective (RMP-1) and nonselective (Fucoidin) selectin blockade.

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