Vol. 284, Issue 1, L224-L231, January 2003
Induction of endotoxin tolerance improves lung function after
warm ischemia in dogs
Ivar
Friedrich1,
Jan
Spillner1,
Er-Xiong
Lu2,
Markus
Barnscheidt2,
Oliver
Kuss3,
Armin
Sablotzki1,
F. Ulrich
Schade2, and
Jochen
Börgermann1
1 Thoracic and Cardiovascular Surgery,
3 Institute of Epidemiology, Biometrics and
Informatics, Martin-Luther-University, 06097 Halle; and
2 Clinical Research Group Shock and Multiorgan
Failure, Essen University, 45128 Essen, Germany
In shock models, induction of
endotoxin tolerance (ET) is known to have a protective effect. The
present study was designed to explore if ET is effective in protecting
lungs from reperfusion injury. Twelve foxhounds were used as
experimental animals. After a left thoracotomy, the left hilum was
clamped for 3 h, followed by 8 h of reperfusion. In the
treatment group (ET, n = 6), dogs were pretreated with
incremental daily endotoxin doses of up to 60 µg/kg on day
6. The ischemia and reperfusion experiment was carried out
on day 9. Control group animals (n = 6) were
not subjected to endotoxin. After 8 h of observation, functional
parameters of the reperfused lung of the ET and the control group were
statistically different (P < 0.05) with respect to
PO2 [ET vs. control: 172.7 ± 12.9 vs.
66.1 ± 7.2 (SE) mmHg], compliance (16.0 ± 1.2 vs. 8.3 ± 1.0 ml/0.1 kPa), and the wet-to-dry ratio (9.4 ± 0.8 vs.
16.7 ± 1.2). After 3 h of warm ischemia and 8 h
of reperfusion, pulmonary function and lung water content improved in
the endotoxin-tolerant group.
ischemia-reperfusion; acute respiratory distress syndrome; surfactant; lipopolysaccharide
