title: Increase of inactive intra-alveolar surfactant subtypes in lungs of asthmatic Brown Norway rats.
abstract: We tested the hypothesis whether allergic airway inflammation in ovalbumin sensitized and challenged Brown Norway rats is associated with intrinsic surfactant alteration and dysfunction. The determination of intra-alveolar surfactant subtypes and alveolar edema within their original microenvironment is only possible using an ultrastructural stereological approach. Therefore both lungs of control and asthmatic rats were fixed by vascular perfusion. The volume fractions of surfactant subtypes and the epithelial surface fraction covered with alveolar edema were determined by point and intersection counting. Furthermore, lung resistance was measured by means of whole-body plethysmography. The surface activity of surfactant from bronchoalveolar lavage was determined as minimum surface tension at minimal bubble size with a pulsating bubble surfactometer. Compared with controls, in asthmatics (1) the fraction of inactive unilamellar forms was significantly increased from 56% to 66%, (2) the fraction of alveolar epithelium covered with alveolar edema visible by light microscopy was significantly increased from 0.7% to 5.0%, (3) the fraction of alveolar epithelium covered with fluid seen by electron microscopy expanded significantly from 5% to 21%, (4) lung resistance was significantly elevated from 14% to 86% and (5) surface tension was enhanced from 6 mN/m to 12 mN/m. Thus, the inflammatory process after allergen challenge of sensitized Brown Norway rats causes intra-alveolar surfactant alterations. These surfactant alterations might contribute to small airway dysfunction.
authors.affiliation: Department of Anatomy, Medical School of Hannover, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany. Schmiedl.Andreas@MH-Hannover.de
authors.forename: A
authors.initials: A
authors.lastname: Schmiedl
authors.forename: H-G
authors.initials: HG
authors.lastname: Hoymann
authors.forename: M
authors.initials: M
authors.lastname: Ochs
authors.forename: A
authors.initials: A
authors.lastname: Menke
authors.forename: A
authors.initials: A
authors.lastname: Fehrenbach
authors.forename: N
authors.initials: N
authors.lastname: Krug
authors.forename: T
authors.initials: T
authors.lastname: Tschernig
authors.forename: J M
authors.initials: JM
authors.lastname: Hohlfeld
mesh_terms: D000280:Administration, Inhalation; D000336:Aerosols; D000818:Animals; D001249:Asthma / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D015824:Blood-Air Barrier / Q000276:immunology; D004195:Disease Models, Animal; D004487:Edema / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D007114:Immunization; D007279:Injections, Subcutaneous; D008168:Lung / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D008297:Male; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology; D011650:Pulmonary Alveoli / Q000378:metabolism* / Q000648:ultrastructure; D011663:Pulmonary Surfactants / Q000378:metabolism*; D051381:Rats; D011914:Rats, Inbred BN; D012129:Respiratory Function Tests
chemical_list: D000336:Aerosols; D011663:Pulmonary Surfactants; D010047:Ovalbumin