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1 Division for Experimental
Perinatal Pathology, Karolinska Hospital, S-171 76 Stockholm,
Sweden; 2 Department of Molecular
Pathology,
Received 27 March 1996; accepted in final form 14 March 1997.
Grossmann, Gertie, Yasuhiro Suzuki, Bengt Robertson, Tsutomu
Kobayashi, Per Berggren, Wen-Zhi Li, Guo-Wei Song, and Bo Sun.
Pathophysiology of neonatal lung injury induced by monoclonal antibody to surfactant protein B. J. Appl.
Physiol. 82(6): 2003-2010, 1997.
animals, newborn; electron microscopy; lung compliance; lung
permeability; respiratory insufficiency
Near-term
newborn rabbits were exposed via the airways to a monoclonal antibody
to surfactant protein B and ventilated for 0-120 min. Control
animals received nonspecific rabbit or mouse immunoglobulin G, saline,
or no material via the airways. Administration of the antibody at
40
mg/kg elicited an immediate, significant fall in lung-thorax compliance
associated with progressive intra-alveolar edema and/or
alveolar collapse and necrosis and desquamation of airway epithelium,
and hyaline membranes. The vascular-to-alveolar leak of human albumin
and human immunoglobulin G, injected intravenously at birth and
determined in lung lavage fluid 60-120 min after instillation of
the antibody, was 1.8% for the left lung, with no difference between
the markers. The average leak in control animals ventilated for 120 min
was <0.3% (P < 0.05). Cytospin preparations of lung lavage fluid from animals exposed to the antibody
showed significantly increased recruitment of neutrophilic granulocytes. The pathology and pathophysiology of neonatal lung injury
induced by the monoclonal antibody to surfactant protein B probably
reflect a combination of direct inactivation of surfactant and an
inflammatory response triggered by the immune reaction.
0161-7567/97 $5.00
Copyright © 1997 the American Physiological Society
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