Atochina E N, Hiemisch H H, Muzykantov V R, Danilov S M
Institute of Experimental Cardiology, Moscow, Russia.
Lung. 1992;170(6):349-58. doi: 10.1007/BF00177581.
The biodistribution of radiolabeled mouse monoclonal antibody (MoAb) to angiotensin-converting enzyme (ACE) and control, nonimmune mouse IgG in platelet activating factor (PAF)-treated rats was studied. The blood level of both preparations was slightly decreased (90% of the control) in PAF-treated rats. Specific pulmonary accumulation of anti-ACE MoAb was reduced to 50% of control in contrast to a doubling in nonspecific pulmonary uptake of non-immune IgG. The changes in anti-ACE MoAb biodistribution were lung-specific and were accompanied by decrease in the pulmonary ACE activity (to 60% of control) and increase in serum ACE activity (to 170% of control). Thus anti-ACE MoAb reveals PAF-induced changes in the status of the pulmonary ACE and therefore can be used for the studies of pathology of the pulmonary endothelium.
研究了放射性标记的抗血管紧张素转换酶（ACE）小鼠单克隆抗体（MoAb）和对照非免疫小鼠IgG在血小板活化因子（PAF）处理的大鼠体内的生物分布。在PAF处理的大鼠中，两种制剂的血液水平均略有下降（为对照的90%）。与非免疫IgG的非特异性肺摄取增加一倍形成对比的是，抗ACE MoAb的特异性肺蓄积减少至对照的50%。抗ACE MoAb生物分布的变化具有肺特异性，并伴有肺ACE活性降低（至对照的60%）和血清ACE活性升高（至对照的170%）。因此，抗ACE MoAb揭示了PAF诱导的肺ACE状态变化，因此可用于研究肺内皮病理学。
