Abstract
Lung injury by oleic acid (OA) or phorbol myristate acetate (20ng/ml) plus polymorphonuclear cells (PMA-PMN) in an ex vivo rabbit shock lung model has been suggested to be caused by OFR production. Using a standard heart/lung preparation with New Zealand rabbits (2.4-4.5 Kg), baseline mean pulmonary artery pressure (PAP) was maintained at 15mmHg and mean airway pressure (MAP) at 10mmHg. Experimental perfusates were infused over 30 minutes followed by Krebs solution. Dimethyl pyroline oxide (DMPO, infused over 30 min) captured OFR which were measured by electron spin resonance. Lung injury was assessed by light and scanning electron microscopy, and lung weight. A five-fold increase in MAP and PAP occurred with both OA and PMA-PMN (p less than 0.003). SOD (20,000 U/kg), but not Vit.A (2,000 IU), prevented lung injury and the increase in OFR with PMA-PMN. We conclude that 1) the mechanism of PMA-PMN lung injury is via OFR because SOD prevents both the rise in OFR and lung injury; 2) Vit.A does not prevent lung injury; 3) OA does not produce injury by increase in OFR but by other unknown mechanisms. We speculate that lung damage by OA and PMA-PMN models have different mechanisms.
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