Scintigraphic evaluation of (123)I-metaiodobenzylguanidine ((123)I-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 (123)I-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 (123)I-MIBG. Pulmonary mean washout rate (WR) of the (123)I-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 (123)I-MIBG and other diagnostic tests for the severity of COPD, such as forced expiratory volume in 1 s (% FEV(1.0): r = 0.386, P < 0.05), carbon monoxide diffusing capacity/alveolar volume (DL(CO)/V(A): r = 0.449, P < 0.01), arterial blood oxygen pressure (PaO(2): r = 0.474, P < 0.01), alveolar-arterial oxygen tension gradient [A-a]DO(2) (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 (123)I-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.