Granulocytes and hyperoxia act synergistically in causing acute lung injury.
Various indirect methods have implicated the polymorphonuclear leukocyte (PMN) as being an important, but not an absolutely necessary, factor in hyperoxia-associated pulmonary edema. By utilizing the cell free isolated perfused rabbit lung model, we demonstrated that the addition of purified, unstimulated granulocytes into the pulmonary artery of hyperoxia exposed lungs resulted in a synergistic edematogenic effect which was statistically significant (p less than 0.05) within only four hours. In addition, significant nonhydrostatic pulmonary edema was produced by both hyperoxia (p less than 0.02) and the addition of PMNs (p = 0.001) when these variables were independently analyzed. These findings help to establish a direct interaction between the role of the PMN and hyperoxia in high permeability lung edema.
D000208:Acute Disease; D000818:Animals; D001835:Body Weight; D006098:Granulocytes / Q000502:physiology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D010100:Oxygen / Q000097:blood*; D010477:Perfusion; D011506:Proteins / Q000378:metabolism; D011654:Pulmonary Edema / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D011817:Rabbits; D007507:Therapeutic Irrigation
D011506:Proteins; D007770:L-Lactate Dehydrogenase; D010100:Oxygen