Role of platelet endothelial cell adhesion molecule-1 in the lung injury caused by mechanical ventilation

ve To investigate the possible role of platelet endothelial cell adhesion molecule-1 (PECAM-1) in the lung injury induced by mechanical ventilation. Methods Twenty-four healthy small pigs of either sex, weighing (17.5±2.5) kg were randomly divided into four groups according to the tida volume of mechanical ventilation: control group without mechanical ventilation; low tidal volume group (A) VT=6 ml·kg-1; normal tidal volume group (B) VT=12ml·kg-1; high tidal volume group (C) VT =25ml·kg-1. The animals were anesthetized with intramuscular ketamine 15-20mg·kg-1 and diazepam 1.5-2.0mg·kg-1 and intubated and mechanically ventilated. Anesthesia was maintained with infusion of ketamine, procaine and succinylcholine. Respiratory rate was set at 18 bpm, I:E=1:2 and FiO2=35% , Femoral artery and vein were cannulated for intra-arterial pressure monitoring, blood sampling and infusion of fluid and anesthetics. ECG, rectal temperature and urine output were monitored. Venous blood samples and lung tissue from right lower lobe were obtained on 1st, 3rd and 7th day of mechanical ventilation for determination of serum and lung myeloperoxidase (MPO) activities, expression of PECAM-1 protein on pulmonary vascular endothelium cells and electron microscopic examination. Results The serum and lung MPO activities were higher in group A, B and C than those in control group (P 0.05 or 0.01) . The PECAM-1 protein expression was down-regulated in group A, B and C as compared with that in control group. Swelling of pulmonary micro-vascular endothelial cells and basement membrane was seen. The gap between the pulmonary micro-vascular endothelial cells was widened significantly. The changes were significant on 7th day, especially in group A and C. Conclusions PECAM-1 may play an important role in the lung injury induced by mechanical ventilation.