title: Infarct-induced chronic heart failure increases bidirectional protein movement across the alveolocapillary barrier.
abstract: Chronic heart failure (CHF) is associated with adaptive structural changes at the alveolocapillary barrier that may be associated with altered protein permeability. Bidirectional protein movement across the barrier was studied in anesthetized rats with infarct-induced CHF by following (125)I-labeled albumin ((125)I-albumin) flux into the alveoli and the leakage of surfactant protein (SP)-B from the alveoli into the circulation. Three groups were studied: controls [0% left ventricular (LV) infarction], moderate infarct (25-45% LV infarction), and large infarct (>46% LV infarction). Wet and dry lung weights increased in the large infarct group (both P < 0.001), consistent with increased lung water and solid lung tissue. (125)I-albumin flux increased across the endothelial (P < 0.001) and epithelial (P < 0.01) components of the alveolocapillary barrier in the large infarct group. Plasma SP-B increased 23% with moderate infarcts (P < 0.05) and 97% with large infarcts (P < 0.001), independent of alveolar levels. Lavage fluid immune cells (P < 0.01) and myeloperoxidase activity (P < 0.05) increased in the large infarct group, consistent with inflammation. Bidirectional protein movement across the alveolocapillary barrier is increased in CHF, and alveolar inflammation may contribute to this pathophysiological defect.
authors.affiliation: Cardiac Services, Department of Critical Care Medicine, Flinders Medical Centre, 5042 Adelaide, South Australia. carmine.depasquale@fmc.sa.gov.au
authors.forename: Carmine G
authors.initials: CG
authors.lastname: De Pasquale
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Bersten
authors.forename: Ian R
authors.initials: IR
authors.lastname: Doyle
authors.forename: Phillip E
authors.initials: PE
authors.lastname: Aylward
authors.forename: Leonard F
authors.initials: LF
authors.lastname: Arnolda
mesh_terms: D000818:Animals; D015824:Blood-Air Barrier / Q000502:physiology*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D002196:Capillaries / Q000502:physiology; D004912:Erythrocytes / Q000378:metabolism; D015633:Extravascular Lung Water / Q000378:metabolism; D006333:Heart Failure / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics / Q000502:physiology; D066298:In Vitro Techniques; D007249:Inflammation / Q000473:pathology; D008168:Lung / Q000737:chemistry / Q000378:metabolism; D008297:Male; D009203:Myocardial Infarction / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D009195:Peroxidase / Q000378:metabolism; D011506:Proteins / Q000378:metabolism*; D011650:Pulmonary Alveoli / Q000378:metabolism*; D011663:Pulmonary Surfactants / Q000378:metabolism; D019275:Radiopharmaceuticals / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015656:Respiratory Mechanics / Q000502:physiology; D012711:Serum Albumin, Radio-Iodinated / Q000378:metabolism; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology
chemical_list: D011506:Proteins; D011663:Pulmonary Surfactants; D019275:Radiopharmaceuticals; D012711:Serum Albumin, Radio-Iodinated; D009195:Peroxidase