Modification by hyperoxia in vivo of endotoxin-induced neutrophil alveolitis in rats. Production of chemotactic factors by alveolar macrophages and ultrastructure.

We have previously shown that prior exposure to hyperoxia intensifies the influx of polymorphonuclear leukocytes into bronchoalveolar spaces after endotoxemia (E), but the mechanism is unknown. Because pulmonary alveolar macrophages (PAM) regulate the migration of polymorphonuclear leukocytes into the lung in several types of acute and chronic alveolitis, we studied the effect of pretreatment with hyperoxia in vivo on production of chemotactic factors by PAM after E. In this study, we cultured PAM recovered by lung lavage from oxygen- and air-pretreated rats 4, 15, and 48 h after E to determine whether a direct effect of hyperoxia on the release of chemotactic factors by PAM in response to E in vivo could contribute to the previous observations. We found that the chemotactic activity of the culture media supernatants from PAM recovered from oxygen-pretreated rats given E was 80% higher than that of media from PAM recovered from air-exposed rats given E. Neither PAM from air-exposed rats nor those from oxygen-exposed rats spontaneously released chemotaxins selective for other PAM. In contrast, when PAM were stimulated with zymosan in vitro, those from the oxygen-breathing group produced 50% more chemotactic activity for other PAM than did those from the air-breathing group. These differences in secretion of chemotactic factors were not associated with decreased viability of PAM either in vivo or in tissue culture, or with impaired adherence by PAM in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)