In vivo evidence of endothelial injury in chronic obstructive pulmonary disease by lung scintigraphic assessment of (123)I-metaiodobenzylguanidine.
In vivo evidence of endothelial injury in chronic obstructive pulmonary disease by lung scintigraphic assessment of (123)I-metaiodobenzylguanidine.
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2003-11
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通讯作者：
T. Arao;N. Takabatake;M. Sata;S. Abe;Y. Shibata;T. Honma;Kazuei Takahashi;A. Okada;Y. Takeishi;I. Kubota
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作者：
T. Arao;N. Takabatake;M. Sata;S. Abe;Y. Shibata;T. Honma;Kazuei Takahashi;A. Okada;Y. Takeishi;I. Kubota
认为肺中（123）I-间碘苄胍（（123）I-MIBG）的未标记闪烁成像评价可识别内皮细胞病变。本研究的目的是阐明肺微血管损伤在慢性阻塞性肺疾病（COPD）发病机制中的作用。方法对25例COPD患者和12例健康对照者进行肺内（123）I-MIBG动力学和临床指标的研究。计算静脉注射123 I-MIBG后30 min（早期显像）和270 min（延迟显像）肺与纵隔平均摄取比值（L/M）。计算了123 I-MIBG的肺平均洗脱率（WR）。结果COPD患者早期和延迟图像的L/M比值及其WR均显著低于对照组（L/M早期：1.26 +/- 0.18 vs. 1.54 +/- 0.11，P < 0.0001; L/M延迟：1.20 +/- 0.12 vs. 1.33 +/- 0.09，P < 0.001; WR：27.4% +/- 5.3%对比34.2% +/-5.7%，P < 0.01）。（123）I-MIBG的肺WR与COPD严重程度的其他诊断性试验（如1 s用力呼气量）之间存在显著相关性% FEV（1.0）：r = 0.386，P < 0.05）、一氧化碳弥散量/肺泡容积（DL（CO）/V（A）：r = 0.449，P < 0.01）、动脉血氧分压（PaO 2：肺动脉血氧分压差[A-a]DO（2）（r =-0.446，P < 0.01）和低密度区百分比（r =-0.458，P < 0.01）。结论由于（123）I-MIBG的肺WR与肺血管表面积的改变无关，提示微血管内皮细胞损伤在COPD的发病中起重要作用。
UNLABELLED 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.