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Respiratory failure in mice caused by a hybridoma making antibodies to the 15 kDa surfactant apoprotein
Author(s) -
Suzuki Y.,
Robertson B.,
Fujita Y.,
Grossmann G.
Publication year - 1988
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1988.tb02730.x
Subject(s) - medicine , lung , edema , pulmonary edema , pathology , respiratory distress , spleen , parenchyma , respiratory system , pulmonary surfactant , antibody , respiratory disease , immunology , anatomy , biology , anesthesia , biochemistry
Hybridoma cells were obtained by fusing spleen cells from mice, immunized against the 15 kDa porcine surfactant apoprotein, with a myeloma cell line. Adult mice were inoculated intraperitoneally with this hybridoma; mice that were not inoculated or were inoculated with myeloma cells served as controls. Lung–thorax compliance was measured at various intervals after inoculation. The animals were then killed for histologic–morphometric evaluation of alveolar air expansion, inflammatory reaction in the pulmonary parenchyma, and intraalveolar edema. In the hybridoma group, the mice developed respiratory failure 9 days after inoculation, with markedly reduced lung–thorax compliance, lung congestion, alveolar collapse, hemorrhagic pulmonary edema, and hyaline membranes. Morphometric data from the same animals showed reduced volume density of alveolar air, and increased volume densities of intraalveolar “fluid” (edema) and tissue components. These lung lesions are similar to those in the adult respiratory distress syndrome.