¹²⁵I–anti-ICAM accumulates without internalization in the isolated rat lungs.

(A) Accumulation of ¹²⁵I–anti-ICAM or¹²⁵I-IgG perfused for 1 hour at 37°C. Inset shows a Scatchard analysis of ¹²⁵I–anti-ICAM binding. (B) Temperature dependence of anti-ICAM uptake (▪) and anti-ACE uptake (■) in the lungs. At 4°C, the pulmonary uptake of¹²⁵I–anti-ACE is inhibited, whereas the uptake of¹²⁵I–anti-ICAM is not affected (uptake at 4°C is shown as percent of the 100% control value attained at 37°C). (C) Disappearance of anti-ICAM (▪) and anti-ACE (■) from the luminal surface in the lungs perfused at 37°C. After accumulation in the lungs, biotin–anti-ICAM, but not biotin–anti-ACE, is accessible to the blood for a prolonged time. ¹²⁵I-streptavidin (¹²⁵I-SA) was perfused in the lungs either immediately after biotinylated antibody accumulation or after 60 minutes of additional perfusion at 37°C with antibody-free buffer. Data of¹²⁵I-SA uptake after 60 minutes delay are shown as percent of that observed immediately after biotinylated antibody accumulation (100% level). All data are shown as means ± SEM; n = 4.