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Endotoxin reduces specific pulmonary uptake of radiolabeled monoclonal antibody to angiotensin-converting enzyme.

Identifieur interne : 005332 ( Main/Exploration ); précédent : 005331; suivant : 005333

Endotoxin reduces specific pulmonary uptake of radiolabeled monoclonal antibody to angiotensin-converting enzyme.

Auteurs : RBID : pubmed:1848608

English descriptors

Abstract

The biodistribution of radiolabeled monoclonal antibody (Mab) to angiotensin-converting enzyme (ACE) was examined in normal and endotoxin-treated rats. Endotoxin administration at a dose of 4 mg/kg induced mild or middle pulmonary edema. The ACE activity in lung homogenate remained virtually unchanged, while the activity of serum ACE increased 15 hr after endotoxin infusion. In normal rats, anti-ACE Mab accumulates specifically in the lung after i.v. injection. Endotoxin injection induces reduction of specific pulmonary uptake of this antibody. Even in non-edematous endotoxemia, the accumulation of anti-ACE Mab antibody (Mab 9B9) decreased from 19.02 to 11.91% of ID/g of tissue without any change in accumulation of control nonspecific IgG. The antibody distribution in other organs and its blood level were almost the same as in the control. In a case of endotoxemia accompanied by increased microvascular permeability, the lung accumulation of Mab 9B9 was reduced to 9.17% of ID/g of tissue, while the accumulation of nonspecific IgG increased to 1.44% versus 0.89% in the control.

PubMed: 1848608

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Le document en format XML

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<title xml:lang="en">Endotoxin reduces specific pulmonary uptake of radiolabeled monoclonal antibody to angiotensin-converting enzyme.</title>
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<name sortKey="Muzykantov, V R" uniqKey="Muzykantov V">V R Muzykantov</name>
<affiliation wicri:level="3">
<nlm:affiliation>Institute of Experimental Cardiology, USSR Cardiology Research Center, Moscow.</nlm:affiliation>
<country>Russie</country>
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<settlement type="city">Moscou</settlement>
<region>District fédéral central</region>
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<wicri:orgArea>Institute of Experimental Cardiology, USSR Cardiology Research Center</wicri:orgArea>
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<author>
<name sortKey="Puchnina, E A" uniqKey="Puchnina E">E A Puchnina</name>
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<author>
<name sortKey="Atochina, E N" uniqKey="Atochina E">E N Atochina</name>
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<author>
<name sortKey="Hiemish, H" uniqKey="Hiemish H">H Hiemish</name>
</author>
<author>
<name sortKey="Slinkin, M A" uniqKey="Slinkin M">M A Slinkin</name>
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<author>
<name sortKey="Meertsuk, F E" uniqKey="Meertsuk F">F E Meertsuk</name>
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<author>
<name sortKey="Danilov, S M" uniqKey="Danilov S">S M Danilov</name>
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<date when="1991">1991</date>
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<term>Antibodies, Monoclonal (pharmacokinetics)</term>
<term>Depression, Chemical</term>
<term>Endotoxins (pharmacology)</term>
<term>Escherichia coli</term>
<term>Humans</term>
<term>Indium Radioisotopes</term>
<term>Iodine Radioisotopes</term>
<term>Isotope Labeling</term>
<term>Lung (drug effects)</term>
<term>Lung (metabolism)</term>
<term>Male</term>
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<term>Peptidyl-Dipeptidase A (immunology)</term>
<term>Rats</term>
<term>Rats, Inbred Strains</term>
<term>Tissue Distribution</term>
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<term>Peptidyl-Dipeptidase A</term>
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<term>Antibodies, Monoclonal</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en">
<term>Endotoxins</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en">
<term>Lung</term>
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<term>Lung</term>
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<term>Animals</term>
<term>Depression, Chemical</term>
<term>Escherichia coli</term>
<term>Humans</term>
<term>Indium Radioisotopes</term>
<term>Iodine Radioisotopes</term>
<term>Isotope Labeling</term>
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<front>
<div type="abstract" xml:lang="en">The biodistribution of radiolabeled monoclonal antibody (Mab) to angiotensin-converting enzyme (ACE) was examined in normal and endotoxin-treated rats. Endotoxin administration at a dose of 4 mg/kg induced mild or middle pulmonary edema. The ACE activity in lung homogenate remained virtually unchanged, while the activity of serum ACE increased 15 hr after endotoxin infusion. In normal rats, anti-ACE Mab accumulates specifically in the lung after i.v. injection. Endotoxin injection induces reduction of specific pulmonary uptake of this antibody. Even in non-edematous endotoxemia, the accumulation of anti-ACE Mab antibody (Mab 9B9) decreased from 19.02 to 11.91% of ID/g of tissue without any change in accumulation of control nonspecific IgG. The antibody distribution in other organs and its blood level were almost the same as in the control. In a case of endotoxemia accompanied by increased microvascular permeability, the lung accumulation of Mab 9B9 was reduced to 9.17% of ID/g of tissue, while the accumulation of nonspecific IgG increased to 1.44% versus 0.89% in the control.</div>
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<Year>1991</Year>
<Month>04</Month>
<Day>19</Day>
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<Year>2004</Year>
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<Day>17</Day>
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<Volume>32</Volume>
<Issue>3</Issue>
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<Year>1991</Year>
<Month>Mar</Month>
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<Title>Journal of nuclear medicine : official publication, Society of Nuclear Medicine</Title>
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<ArticleTitle>Endotoxin reduces specific pulmonary uptake of radiolabeled monoclonal antibody to angiotensin-converting enzyme.</ArticleTitle>
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<AbstractText>The biodistribution of radiolabeled monoclonal antibody (Mab) to angiotensin-converting enzyme (ACE) was examined in normal and endotoxin-treated rats. Endotoxin administration at a dose of 4 mg/kg induced mild or middle pulmonary edema. The ACE activity in lung homogenate remained virtually unchanged, while the activity of serum ACE increased 15 hr after endotoxin infusion. In normal rats, anti-ACE Mab accumulates specifically in the lung after i.v. injection. Endotoxin injection induces reduction of specific pulmonary uptake of this antibody. Even in non-edematous endotoxemia, the accumulation of anti-ACE Mab antibody (Mab 9B9) decreased from 19.02 to 11.91% of ID/g of tissue without any change in accumulation of control nonspecific IgG. The antibody distribution in other organs and its blood level were almost the same as in the control. In a case of endotoxemia accompanied by increased microvascular permeability, the lung accumulation of Mab 9B9 was reduced to 9.17% of ID/g of tissue, while the accumulation of nonspecific IgG increased to 1.44% versus 0.89% in the control.</AbstractText>
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