Vol. 284, Issue 6, H2136-H2145, June 2003
Infarct-induced chronic heart failure increases bidirectional
protein movement across the alveolocapillary barrier
Carmine G.
De
Pasquale1,
Andrew D.
Bersten2,
Ian R.
Doyle3,
Phillip E.
Aylward1, and
Leonard F.
Arnolda4
1 Cardiac Services, 2 Department of
Critical Care Medicine, Flinders Medical Centre, and
3 Department of Human Physiology, Flinders University,
5042 Adelaide, South Australia; and 4 Cardiology
Department, Royal Perth Hospital and West Australian
Institute of Medical Research, 6000 Perth, Western Australia,
Australia
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
125I-labeled albumin (125I-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.
125I-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.
alveolocapillary barrier permeability; cardiogenic pulmonary edema; surfactant protein B; albumin permeability
