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Despite marked improvements in antibiotic therapy, the accurate diagnosis and treatment of bacterial lower respiratory tract infection remain a challenge. The bronchoscopic protected specimen brush and bronchoscopic bronchoalveolar lavage combined with quantitative bacterial cultures can provide sensitive and relatively specific information about lower airway flora. Both of these methods require strict observance of the required protocol, careful processing of the obtained specimens, and the absence of prior antibiotic therapy to obtain best results. These procedures are also of some utility in sickle cell acute chest syndrome, bronchiectasis, and in the immunocompromised host.

Isolated perfused rat lungs were subjected to oxidant injury induced by tert-butyl hydroperoxide (t-buOOH), which caused a significant increase in capillary permeability as assessed by the change in the capillary filtration coefficient. t-buOOH caused an increase in the change in the capillary filtration coefficient (delta Kfc) of 0.27 +/- 0.05 ml.min.cmH2O-1.100 g lung tissue-1 (mean +/- SE) that was accompanied by an increase in thiobarbituric acid reactive products of lipid peroxidation in the lung perfusate. The addition of hemoglobin to the perfusate potentiated t-buOOH-induced lung injury as evidenced by a significantly greater (P = 0.007) delta Kfc of 0.43 +/- 0.05. t-buOOH also caused hemoglobin to release large quantities of free iron in vitro. The potentiation of t-buOOH-induced lung injury by hemoglobin was prevented by apotransferrin as evidenced by a significant reduction (P = 0.001) in delta Kfc to 0.13 +/- 0.02. No statistically significant (P greater than 0.05) changes in segmental resistances or pulmonary vascular pressures occurred in any of the lungs injured with t-buOOH when compared with time controls. These results demonstrate that t-buOOH causes an oxidant injury in isolated rat lungs that can be potentiated by free iron released from hemoglobin.

Toxic oxygen species are thought to play a primary role in the pathophysiological mechanisms responsible for a diverse group of lung diseases. In this study, isolated perfused rat lungs were subjected to oxidant injury induced by ischemia-reperfusion (IR) and t-butyl hydroperoxide (t-buOOH) challenge. Both forms of injury caused large increases in capillary permeability as assessed by the capillary filtration coefficient (Kfc). IR and t-buOOH challenge caused increases in the Kfc of 0.95 +/- 0.22 and 0.30 +/- 0.06 ml.min-1.cmH2O-1.100 g lung tissue-1, respectively. U74500A, a potent inhibitor of iron-mediated lipid peroxidation, significantly attenuated the endothelial damage seen in both forms of injury. In lungs pretreated with U74500A, the Kfc increased 0.01 +/- 0.02 and 0.11 +/- 0.03 ml.min-1.cmH2O-1.100 g lung tissue-1 following IR and t-buOOH challenge, respectively. In lungs pretreated with the iron binding protein transferrin the Kfc increased 0.31 +/- 0.11 and 0.19 +/- 0.03 ml.min-1.cmH2O-1.100 g lung tissue-1 following IR and t-buOOH challenge, respectively. In these studies, transferrin significantly attenuated permeability in the IR group only. However, the attenuation of injury in IR due to U74500A was significantly greater (P less than 0.05) than the attenuation provided by transferrin. Both forms of injury also caused small but statistically significant increases in pulmonary artery pressure. These results suggest that the increase in capillary permeability seen after IR and t-buOOH is in part mediated by iron-dependent mechanisms.