Pulmonary bacterial clearance and alveolar macrophage function in septic shock lung.

The association between the pulmonary bacterial clearance and the development of septic shock lung has been demonstrated in porcine and canine experimental models. In order to elucidate the role of the pulmonary reticuloendothelial system in bacterial clearance, the functions of alveolar macrophages (AM) obtained by bronchopulmonary lavage were studied. Five piglets were infused intravenously with Pseudomonas aeruginosa labeled with tritiated thymidine at 3 to 6 X 10(8) CFU/kg/min. Septic shock and manifestations like those of the adult respiratory distress syndrome developed within 1 h, and the pigs died within 2 to 3 h. Pulmonary bacterial clearance was 93% initially, and progressively decreased to 29%, as Pao2 decreased and lung water increased. The number of bacteria in the serial lung biopsy specimens increased steadily, although the distribution was not homogeneous. Differential centrifugations, repeated washings, and scintillation countings of the lavage fluid showed that in vivo AM phagocytosis was nil, despite the abundant bacteria found in the lavage fluid. However, when these AM were washed and tested in vitro in the presence of optimal concentrations of opsonin and oxygen, their phagocytic capability was well preserved, and was not significantly different from that of prebacterial infusion baseline values. It is concluded that in the septic shock lung, the lung clears bacteria not primarily by AM uptake but by other mechanisms, such as mechanical leakage into the pulmonary space, or by pulmonary intravascular leukocyte uptake. The apparent AM dysfunction in vivo is not intrinsic, and is likely to be caused by microenvironmental factors, such as lack of adequate opsonin and oxygen.