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pubmed-article:1331624pubmed:abstractTextThe 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.lld:pubmed
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pubmed-article:1331624pubmed:pagination349-58lld:pubmed
pubmed-article:1331624pubmed:dateRevised2003-11-14lld:pubmed
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pubmed-article:1331624pubmed:articleTitleSystemic administration of platelet-activating factor in rat reduces specific pulmonary uptake of circulating monoclonal antibody to angiotensin-converting enzyme.lld:pubmed
pubmed-article:1331624pubmed:affiliationInstitute of Experimental Cardiology, Moscow, Russia.lld:pubmed
pubmed-article:1331624pubmed:publicationTypeJournal Articlelld:pubmed
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