Sequential Assessment of Pulmonary Epithelial Diethylene Triamine Penta-acetate Clearance and Intrapulmonary Transferrin Accumulation duringEscherichia coliPeritonitis

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Abstract
The individual roles of pulmonary capillary endothelial and alveolar epithelial permeability in the pathogenesis of the adult respiratory distress syndrome (ARDS) are unclear. We developed a method for the sequential assessment of pulmonary macromolecule accumulation and small solute clearance in vivo using a gamma camera. We measured the exponential clearance coefficient of 111In-labeled diethylene triamine penta-acetate (111In-DTPA) to assess airway clearance of small solutes. We also calculated the exponential equilibration coefficient of 111In-labeled transferring (111In-TF) to assess intrapulmonary accumulation of transferrin. We determined these parameters in guinea pigs with Escherichia coli peritonitis and compared them with a saline-treated control group, oleic-acid-treated groups, and a group treated with low molecular weight dextran Ringer solution. The pulmonary DTPA clearance and the intrapulmonary transferrin accumulation were significantly increased in the peritonitis group (29.4 .+-. 8.2 .times. 10-3 min-1, p < 0.02, and 15.1 .+-. 3.1 .times. 10-3 min-1, p < 0.02) when compared with the control group (3.1 .+-. 0.8 .times. 10-3 min-1 and 4.5 .+-. 0.5 .times. 10-3 min-1). These changes developed within 5.5 h of the initial insult. Neither increased extravascular lung water nor elevated pulmonary artery and left atrial pressures were detected in the peritonitis group. The low molecular weight dextran Ringer group did not show a significant increase in the pulmonary DTPA clearance and the intrapulmonary transferrin accumulation. The E. coli peritonitis and oleic-acid-treated groups showed different slopes of correlation between the exponential clearance coefficient of DTPA and the exponential equilibration coefficient of transferrin, suggesting that these insults may create different patterns of pulmonary epithelial and endothelial damage. This raises the possibility that lung injury from different insults may be distinguishable by different patterns of injury. We conclude that this technique of sequential assessment of pulmonary 111In-DTPA clearance and intrapulmonary accumulation of 111In-TF may detect alveolar septal membrane damage early in the pathogenesis of acute lung injury.