Systemic administration of platelet-activating factor in rat reduces specific pulmonary uptake of circulating monoclonal antibody to angiotensin-converting enzyme.
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.
Atochina
E N
EN
Institute of Experimental Cardiology, Moscow, Russia.
Hiemisch
H H
HH
Muzykantov
V R
VR
Danilov
S M
SM
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology*; D004730:Endothelium, Vascular / Q000276:immunology; D008168:Lung / Q000187:drug effects* / Q000276:immunology; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000276:immunology*; D010972:Platelet Activating Factor / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar
D000911:Antibodies, Monoclonal; D010972:Platelet Activating Factor; D007703:Peptidyl-Dipeptidase A