RT Journal Article SR Electronic T1 In Vivo Evidence of Endothelial Injury in Chronic Obstructive Pulmonary Disease by Lung Scintigraphic Assessment of 123I-Metaiodobenzylguanidine JF Journal of Nuclear Medicine JO J Nucl Med FD Society of Nuclear Medicine SP 1747 OP 1754 VO 44 IS 11 A1 Tsuyoshi Arao A1 Noriaki Takabatake A1 Makoto Sata A1 Shuichi Abe A1 Yoko Shibata A1 Tsuguo Honma A1 Kazuei Takahashi A1 Akio Okada A1 Yasuchika Takeishi A1 Isao Kubota YR 2003 UL http://jnm.snmjournals.org/content/44/11/1747.abstract AB Scintigraphic evaluation of 123I-metaiodobenzylguanidine (123I-MIBG) in the lungs is considered to recognize endothelial cell lesions. The aim of this study was to clarify the involvement of the pulmonary microvascular injury in the pathogenesis of chronic obstructive pulmonary disease (COPD). Methods: We investigated lung 123I-MIBG kinetics and clinical indices in 25 COPD patients and 12 control subjects. Mean uptake ratios of lung to mediastinum (L/M) were calculated in anterior planer images at 30 min (early image) and 270 min (delayed image) after intravenous injection of 123I-MIBG. Pulmonary mean washout rate (WR) of the 123I-MIBG was also calculated. Results: The L/M ratios in both early and delayed images of COPD patients, as well as its WR, were significantly lower than those of the control subjects (L/M early: 1.26 ± 0.18 vs. 1.54 ± 0.11, P < 0.0001; L/M delayed: 1.20 ± 0.12 vs. 1.33 ± 0.09, P < 0.001; WR: 27.4% ± 5.3% vs. 34.2% ± 5.7%, P < 0.01). There were significant relationships between lung WR of the 123I-MIBG and other diagnostic tests for the severity of COPD, such as forced expiratory volume in 1 s (% FEV1.0: r = 0.386, P < 0.05), carbon monoxide diffusing capacity/alveolar volume (DLCO/VA: r = 0.449, P < 0.01), arterial blood oxygen pressure (Pao2: r = 0.474, P < 0.01), alveolar–arterial oxygen tension gradient [A–a]Do2 (r = −0.446, P < 0.01), and percentage of low-attenuation area (r = −0.458, P < 0.01) in the study population. Conclusion: Because lung WR of the 123I-MIBG is considered to be independent of an alteration of the pulmonary vascular surface area, these results suggest that the microvascular endothelial cell injury plays a significant role in the pathogenesis of COPD.