Watts F L, Oliver B L, Johnson G M, Thrall R S
Department of Anesthesiology, University of Connecticut Health Center, Farmington 06032.
Free Radic Biol Med. 1990;9(4):327-32. doi: 10.1016/0891-5849(90)90007-6.
The purpose of this study was to investigate the superoxide anion (O2-)-generating capacity of neutrophils isolated from rats at various stages of oleic acid(OA)-induced lung injury. Neutrophils were collected from blood, bronchoalveolar lavage (BAL), and peritoneal cavity (glycogen induced) after OA administration. Control neutrophils were collected from the blood of normal animals as a representative of nonprimed cells that produce low levels of O2-. A second control was the glycogen-elicited peritoneal neutrophil of normal animals which represented primed cells that produce enhanced levels of O2-. The ability of the neutrophils to produce O2- was evaluated by using both myristate acetate and opsonized zymosan as stimulants. Neutrophils isolated from blood and BAL from OA-injured lungs produced low levels of O2- and resembled closely the circulating, nonprimed neutrophil. Myeloperoxidase levels were measured in plasma and BAL and were found to be elevated in BAL of OA-injured animals. The inability of neutrophils to produce high levels of O2- and the elevation of myeloperoxidase suggest that neutrophils present in the lung may have degranulated in response to prior activation and are therefore incapable of further superoxide production.