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123I-IMP is taken up by the pulmonary capillary endothelial cells during the first pass through the lung, and is slowly released from them. To look up the factors which influence on the prolonged 123I-IMP retention in the diseased lung, we examined the correlation between the 123I-IMP uptake during the first pass and the 123I-IMP retention. Patients with bronchial asthma had no abnormal finding in the chest X-ray photograph. However 123I-IMP release from their lungs was delayed. Some patients show a tendency that 123I-IMP uptake during the first pass was uneven, which suggested the change in amine uptake function of endothelial cells. However their correlation coefficients between the uptake during the first pass and the prolonged retention were very small. It was considered that the prolonged 123I-IMP retention in the diseased lung was not explained only by the change in uptake function of pulmonary capillary endothelial cell.

The movement of N-isopropyl-p[123I] iodoamphetamine (I-123 IMP) in the lungs was studied. The half time of I-123 IMP release (T 1/2) was delayed in the fibrosis and the sarcoidosis. There was a relation between the prolongation of T 1/2 and the radiographic finding. It was considered that T 1/2 was useful for the objective estimation of the change in the lungs. The adsorption of I-123 IMP to the alveolar cells was much higher than to the circulating leukocytes. It was considered that the accumulation and retention of I-123 IMP in the lungs had relation to the alveolar cells.

The accumulation of venously injected 123I-IMP in the lung was studied. Between 30 and 50 min after the injection of the 1.5 mCi 123I-IMP, the concentration of 123I-IMP in the broncho-alveolar lavage fluid were much higher than in the blood. It was considered that 123I-IMP was transported into the alveolar spaces and was absorbed by the alveolar cells. The half time (T1/2) of the 123I-IMP release from the lung between 10 and 25 min immediately after the injection was calculated. In normal subjects the T1/2 ranged between 25 and 44 min and was prolonged in subjects with pulmonary fibrosis, sarcoidosis, and allergic alveolitis. It was considered that the retention of 123I-IMP was related not only to the endothelial cells, but also to the alveolar cells. It was considered that the analysis of the lung release of 123I-IMP forms a new lung dysfunction index.