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Systemic administration of platelet-activating factor in rat reduces specific pulmonary uptake of circulating monoclonal antibody to angiotensin-converting enzyme

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Abstract

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.

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Authors and Affiliations

  1. Institute of Experimental Cardiology, 3rd Cherepkovskaja Street, 15a, 121552, Moscow, Russia

    Elena N. Atochina, Holger H. Hiemisch, Vladimir R. Muzykantov & Sergei M. Danilov

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  1. Elena N. Atochina
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  2. Holger H. Hiemisch
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  3. Vladimir R. Muzykantov
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  4. Sergei M. Danilov
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Atochina, E.N., Hiemisch, H.H., Muzykantov, V.R. et al. Systemic administration of platelet-activating factor in rat reduces specific pulmonary uptake of circulating monoclonal antibody to angiotensin-converting enzyme. Lung 170, 349–358 (1992). https://doi.org/10.1007/BF00177581

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