CHARACTERIZATION OF PULMONARY CELLULAR INFLUX DIFFERENTIALS TO KNOWN TOXIC AGENTS BETWEEN SPECIES

Chickens, frogs and toads were resistant to acute pulmonary injury by a variety of toxic agents (O2, hyperbaric O2, paraquat, and silica) that caused extensive acute injury in mammals. Acute pulmonary injury was defined as a massive influx of inflammatory cells, interstitially and into the alveolar spaces, pulmonary edema, hemorrhage and the presence of H2O2 and O2- in the lavaged supernatant, occurring within 48 h. In some cases, chronic effects of the toxins were observed after 90 h, i.e., hemorrhage, fibrosis and an accumulation of interstitial inflammatory cells. In all 3 nonmammal systems, isolated inflammatory cells failed to respond chemotactically in vitro to known mammalian chemotaxins. Pulmonary lavage of the exposed chickens, frogs and toads also failed to produce inflammatory cells. Pulmonary edema was not deteced in any animal by comparison of lung weight to total body weight. Intratracheal injections of silica for 2 wk did produce chronic effects in chickens and frogs. Morphologically, the lungs showed signs of fibrosis and accumulation of interstitial inflammatory cells, but no intraalveolar cells. After 90 h of hyperbaric O2, frogs exhibited a massive infiltration of interstitial inflammatory cells and hemorrhage. Elevated O2 levels (100%) for 2 wk under normal atmospheric conditions produced no changes in frog lungs or in the amount of inflammatory cells in the lungs. I.v. injections of paraquat for up to 208 h failed to initiate an accumulation of pulmonary inflammatory cells or the development of pulmonary edema in chickens. There was also no detectable H2O2 of O2- in the lavaged supernatant. It was not determined whether paraquat had a longer or more chronic effect on chickens. The lack of an acute pulmonary inflammatory mechanism in chickens, frogs and toads was partly responsible for the resistance of these animals to acute pulmonary injury by oxidizing mammalian toxins.